Right Heart Catheterization: Swan-Ganz Catheter презентация

Содержание

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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 invention of the catheter is said to have derived from watching the wind playing with sails in Santa Monica.

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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 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.

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Swan-Ganz Catheter

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The Pulmonary Artery Catheter: Swan-Ganz Catheter

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Principal 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

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Right Heart Catheterization

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0

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

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Right Atrium

Right Ventricle

Pulmonary Artery

PC Wedge

Rt Heart Catheterization

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Jugular 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

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0

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

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Normal Cardiac Hemodynamics (Adult)

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Normal 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 %

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Oxygen Parameters

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Normal 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

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Measured 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

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Calculated Variables

Cardiac index
Stroke index
Systemic vascular resistance
Pulmonary vascular resistance
Shunts
Ventricular function
Valvular stenosis or regurgitation

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Stenotic Orifices

Gradients
Valve orifice cross-sectional areas
Measurements assist in making decisions regarding surgical intervention

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Mitral Stenosis

Diastolic gradient from the left atrium to the left ventricle
Atrial myxoma may

produce similar findings

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Cardiac Output

Three main invasive methods of measurement
Flick method
Indicator-dilution method
Angiographic method

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Fick 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)

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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

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Cardiac Output (High)

Acute
Acute hypervolemia
ARDS, severe pneumonia
Septic shock
Acute intoxications
Fever, heat stress, malignant hyperthermia
Anxiety,

emotional stress
Delirium tremens

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Cardiac Output (High)

Chronic
Severe chronic anemia
Cirrhosis
Chronic renal failure
Pregnancy
Thyrotoxicosis
Polycythemia vera
Labile hypertension
Congenital heart disease (PDA)

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Cardiac 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

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Cardiac Output (Low)

Acute
Arrhythmias
Sustained VT
Extreme bradycardia
Acute inotropic changes in a failing myocardium
Beta-blockers
Ischemia
Acidosis

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Cardiac 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

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Shunts

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

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Shunts

Evaluation of shunts requires:
Detection
Classification
Localization
Quantitation

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Left 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

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Right 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

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Pulmonary Hypertension: Role of Right Heart Catheterization

For diagnosis
For evaluating acute vasodilator response
For evaluating

progression
For treatment selection
Lung vs. heart-lung transplantation

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PAH: Hemodynamic Definition

PA = pulmonary artery; PVR = pulmonary vascular resistance;
TPG =

transpulmonary gradient

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PAH 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

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Swan-Ganz Catheter Related Complications

Harvey S et al. The Lancet 2005; 366:472-477

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Wiggers Diagram

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Left 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

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Vascular Access: Left Heart Cath

Sones’ technique (brachial approach)
Judkin’s technique (femoral approach)
Radial approach

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Left Heart Catheterization

Coronary angiography
Left ventriculogram
Ascending aortogram
Pressure measurements in LV/aorta

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Cardiac 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

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Wall Motion Abnormalities

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Aortic Stenosis

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Coronary Anatomy

Depending on coronary anatomy: 1 VD, 2 VD and 3 VD; LMCA

disease

mm

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Treatment 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

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Percutaneous Coronary Interventions (PCI)

1977: 1st Coronary angioplasty by Gruntzig
Limitation: restenosis

1939-1985

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PCI 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.

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Treatment 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%)

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Treatment 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)

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STEMI: 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

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Baseline LAO

Baseline LAO/Cranial

Baseline RAO

Baseline Angiogram of Patient with Prolonged Anginal Pain and ST-elevation

in leads II, III and AVF

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Post PTCA with stent

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Left 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

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Contrast 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

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Risk Factors for the Development of Contrast-Induced Nephropathy

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Treatment Modalities Assessed in Randomized Trials on Prevention of CIN

+ positive effect;

– no effect; +/– conflicting data

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Intraaortic Balloon

Catheter
Inner Pressure Lumen
Gas Shuttle Lumen
Catheter Tip
Membrane
Sheath

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• ↓ Cardiac Work
• ↓ Myocardial O2 Consumption
• ↑ Cardiac Output

Principles of Counterpulsation Systole:

IAB Deflation

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Impella Device

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SYNERGY

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

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Dynamics 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

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Mechanical Heart Failure Devices

Mancini D, Burkoff D, Circulation, 2005;112:438-446

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PARTNER 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%.

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All-Cause Mortality Landmark Analysis

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Catheter-Based Mitral Valve Repair: MitraClip® System

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Investigational 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

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