Right Heart Catheterization: Swan-Ganz Catheter презентация

Содержание

Слайд 2

Right Heart Catheterization Swan-Ganz Catheter: History Jeremy Swan (1922-2005), an

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.
Слайд 3

Swan-Ganz Catheter: History Jeremy Swan (1922-2005), an Irish cardiologist, worked

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.

Слайд 4

Swan-Ganz Catheter

Swan-Ganz Catheter

Слайд 5

The Pulmonary Artery Catheter: Swan-Ganz Catheter

The Pulmonary Artery Catheter: Swan-Ganz Catheter

Слайд 6

Principal Indications for Swan-Ganz Catheter Shock of unclear etiology (cardiogenic,

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
Слайд 7

Right Heart Catheterization

Right Heart Catheterization

Слайд 8

0 100 200 300 400 500 600 700 800 0

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

Слайд 9

Right Atrium Right Ventricle Pulmonary Artery PC Wedge Rt Heart Catheterization

Right Atrium

Right Ventricle

Pulmonary Artery

PC Wedge

Rt Heart Catheterization

Слайд 10

Jugular Venous Pulsations A wave – backward flow of blood

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
Слайд 11

Слайд 12

Слайд 13

Слайд 14

Слайд 15

Слайд 16

0 100 200 300 400 500 600 700 800 0

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

Слайд 17

Слайд 18

Normal Cardiac Hemodynamics (Adult)

Normal Cardiac Hemodynamics (Adult)

Слайд 19

Normal Cardiac Hemodynamics (Adult) Fick CO CO 3.5 – 8.5

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 %
Слайд 20

Oxygen Parameters

Oxygen Parameters

Слайд 21

Normal Pressures LA and PCW: Mean 4-12mmHg Aorta: Systolic 90-140mmHg

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
Слайд 22

Measured Variables Mean and phasic arterial blood pressure Heart rate

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
Слайд 23

Calculated Variables Cardiac index Stroke index Systemic vascular resistance Pulmonary

Calculated Variables

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

or regurgitation
Слайд 24

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

Stenotic Orifices

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

intervention
Слайд 25

Слайд 26

Mitral Stenosis Diastolic gradient from the left atrium to the

Mitral Stenosis

Diastolic gradient from the left atrium to the left ventricle
Atrial

myxoma may produce similar findings
Слайд 27

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

Cardiac Output

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

Слайд 28

Fick Method The amount of oxygen extracted by the lungs

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)
Слайд 29

The Indicator-dilution Technique and Thermodilution Technique Dilution of an indicator

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 30

Cardiac Output (High) Acute Acute hypervolemia ARDS, severe pneumonia Septic

Cardiac Output (High)

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

malignant hyperthermia
Anxiety, emotional stress
Delirium tremens
Слайд 31

Cardiac Output (High) Chronic Severe chronic anemia Cirrhosis Chronic renal

Cardiac Output (High)

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

(PDA)
Слайд 32

Cardiac Output (Low) Acute Acute hypovolemia (absolute or relative) Acute

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
Слайд 33

Cardiac Output (Low) Acute Arrhythmias Sustained VT Extreme bradycardia Acute

Cardiac Output (Low)

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

Слайд 34

Cardiac Output (Low) Chronic Chronic severe pulmonary hypertension Chronic myocardial

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
Слайд 35

Shunts Demonstrated by an absence of an expected pressure difference

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
Слайд 36

Shunts Evaluation of shunts requires: Detection Classification Localization Quantitation

Shunts

Evaluation of shunts requires:
Detection
Classification
Localization
Quantitation

Слайд 37

Left to Right Shunts Mixing of saturated (systemic arterial or

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
Слайд 38

Right to Left Shunts Mixing of desaturated (systemic venous or

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
Слайд 39

Pulmonary Hypertension: Role of Right Heart Catheterization For diagnosis For

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
Слайд 40

PAH: Hemodynamic Definition PA = pulmonary artery; PVR = pulmonary vascular resistance; TPG = transpulmonary gradient

PAH: Hemodynamic Definition

PA = pulmonary artery; PVR = pulmonary vascular resistance;


TPG = transpulmonary gradient
Слайд 41

PAH Hemodynamic Calculations TPG: Transpulmonary gradient = PAmean – PCWmean

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
Слайд 42

Swan-Ganz Catheter Related Complications Harvey S et al. The Lancet 2005; 366:472-477

Swan-Ganz Catheter Related Complications

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

Слайд 43

Wiggers Diagram

Wiggers Diagram

Слайд 44

Left Heart Catheterization: History First human catheterization by Werner Forssmann:

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
Слайд 45

Vascular Access: Left Heart Cath Sones’ technique (brachial approach) Judkin’s technique (femoral approach) Radial approach

Vascular Access: Left Heart Cath

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

approach
Слайд 46

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

Left Heart Catheterization

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

Слайд 47

Cardiac Angiography: Ventriculography A contrast roadmap of the left ventricle

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
Слайд 48

Wall Motion Abnormalities

Wall Motion Abnormalities

Слайд 49

Aortic Stenosis

Aortic Stenosis

Слайд 50

Coronary Anatomy Depending on coronary anatomy: 1 VD, 2 VD and 3 VD; LMCA disease mm

Coronary Anatomy

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

VD; LMCA disease

mm

Слайд 51

Treatment Strategies of CAD Medical treatment, PCI or CABG -

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
Слайд 52

Percutaneous Coronary Interventions (PCI) 1977: 1st Coronary angioplasty by Gruntzig Limitation: restenosis 1939-1985

Percutaneous Coronary Interventions (PCI)

1977: 1st Coronary angioplasty by Gruntzig
Limitation: restenosis

1939-1985

Слайд 53

PCI Procedural refinements: Stents Expandable metal mesh tubes that buttresses

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.
Слайд 54

Treatment Strategies of CAD Stable angina Unstable angina/non ST-elevation MI

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%)
Слайд 55

Treatment Strategies of CAD Stable angina Unstable angina/non ST-elevation MI

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)
Слайд 56

STEMI: PCI vs. Thrombolysis Advantages of PCI Knowledge of CA

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

Слайд 57

Baseline LAO Baseline LAO/Cranial Baseline RAO Baseline Angiogram of Patient

Baseline LAO

Baseline LAO/Cranial

Baseline RAO

Baseline Angiogram of Patient with Prolonged Anginal Pain

and ST-elevation in leads II, III and AVF
Слайд 58

Post PTCA with stent

Post PTCA with stent

Слайд 59

Left Heart Catheterization: Complications Early: Death: 0.1-0.2% Acute MI :

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
Слайд 60

Contrast Induced Nephropathy: Pathogenesis Hemodynamic changes Reduction renal blood flow

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

Слайд 61

Risk Factors for the Development of Contrast-Induced Nephropathy

Risk Factors for the Development of Contrast-Induced Nephropathy

Слайд 62

Treatment Modalities Assessed in Randomized Trials on Prevention of CIN

Treatment Modalities Assessed in Randomized Trials on Prevention of CIN

+

positive effect; – no effect; +/– conflicting data
Слайд 63

Intraaortic Balloon Catheter Inner Pressure Lumen Gas Shuttle Lumen Catheter Tip Membrane Sheath

Intraaortic Balloon

Catheter
Inner Pressure Lumen
Gas Shuttle Lumen
Catheter Tip
Membrane
Sheath

Слайд 64

• ↓ Cardiac Work • ↓ Myocardial O2 Consumption •

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

Principles

of Counterpulsation Systole: IAB Deflation
Слайд 65

Impella Device

Impella Device

Слайд 66

SYNERGY 1994 1995 1996 1997 1998 1999 2000 2002 2003

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

Слайд 67

Dynamics of Antithrombotic Therapy in Patients with ACS and Patients

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

Слайд 68

Mechanical Heart Failure Devices Mancini D, Burkoff D, Circulation, 2005;112:438-446

Mechanical Heart Failure Devices

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

Слайд 69

PARTNER Study Design N = 358 Inoperable Standard Therapy n

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%.

Слайд 70

All-Cause Mortality Landmark Analysis

All-Cause Mortality Landmark Analysis

Слайд 71

Catheter-Based Mitral Valve Repair: MitraClip® System

Catheter-Based Mitral Valve Repair: MitraClip® System

Слайд 72

Investigational Device only in the US; Not available for sale

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

Имя файла: Right-Heart-Catheterization:-Swan-Ganz-Catheter.pptx
Количество просмотров: 23
Количество скачиваний: 0