Iabp principle, hemodynamic, timing, weaning 2016 background asmiha,isman edit - [PDF Document] (2024)

Dr. Isman Firdaus, SpJP(K), FIHA, FESC, FAPSIC,FSCAIEmail: [emailprotected]

Position and Organization :• Critical care and Interventional Cardiologist Consultant National Cardiovascular Center,

Harapan Kita Hospital• Executive Board Member of Indonesian Heart Association (IHA)• Excutive Board Member of WG Acute Cardiac Care-IHA• Member of Acute Cardiac Care Association-European Society of Cardiology (ACCA-ESC).• Member of European Association of Percutaneous Coronary Intervention (EAPCI-ESC)• Member of European Rescucitation Council (ERC)• Fellow of European Society of Cardiology (FESC)• Fellows of Asia Pacific Society of Interventional Cardiologist (FAPSIC)• Fellow of Society Catheterization Angiography and Intervention (FSCAI)• Asia Pacific advisory board of Heart Failure

Pekerjaan :• Staf Pengajar Departemen Kardiologi Fakultas Kedokteran UI• Cardiovascular intensivist-intervensionist consultant RS Jantung Harapan Kita

Curricullum Vitae

Intra Aortic Balloon Pump:Basic Principle

Isman Firdaus, MD, FIHA, FAPSIC, FESC, FSCAI

National Cardiovascular Center Harapan Kita

Mortality: Major Shock Categories

J Am Coll Cardiol 2000;36:1063–70

Intra-aortic Balloon Pump(IABP)

• IABP first successfully used by Kantrowitz et al. in

1967

• Able to reverse pharmacologically refractory Post MI

cardiogenic shock using this technique

• Kantrowitz et al. Initial clinical experience with

intraaortic balloon pumping in cardiogenic shock.

JAMA 203:135, 1968

Basics of Cardiac Physiology

• Determinants of myocardial O2 delivery

• Determinants of myocardial O2 consumption

• Determinants of Cardiac Output

• Windkessel Effect

Determinants of Myocardial DO2

• MVO2 = CBF X (CaO2-CvO2) Fick Principle

• heart has near maximal extraction at rest. Increased needs are

met by increased O2 delivery.

• O2 delivery is regionally controlled by autoregulation,

• Ischemic heart has maximally dilated arteries. Perfusion is

then directly related to perfusion pressure.

• Coronary perfusion occurs predominately during diastole

• Increasing diastolic time increases coronary blood flow

Fick Principle

MVO2 = CBF X (CaO2-CvO2)

• CBF : coronary blood flow (ml/mnt)• CaO2 : Ox Content in arterial• CvO2: Ox content in vein• Art-Vein Ox Diff: CaO2 –CvO2

Ex/ CBF 80 ml/mntCaO2-CvO2= 0,1 ml/mnt bloodMVO2 = 8 ml O2/mnt per gram

Determinants of Myocardial DO2(cont’)

• Major resistance to (subendocardial) coronary blood flow

during diastole is LVEDP such that...

• CPP=AoDP-LVEDP

• AoDP and LVEDP are dynamic values

• Overlapping the aortic pressure and LV pressure curves gives a

visual representation of the pressure gradient.

• This gradient over the diastolic time cycle is described as the

Diastolic Pressure Time Index (DPTI)

• Area within the DPTI is directly correllated with O2

availability to the myocardium (supply)

Determinants of MVO2

• HR, contractility, wall tension (50% of MVO2 at rest).

• Laplace’s law T=Pr/2h

• Intraventricular pressure is a modifiable variable.

• IVP greatest during systole (LVSP).

• LVSP is a dynamic value continually changing throughout

systole and altering wall tension as this occurs.

• Area under the LVSP tracing is represented by the Tension

Time Index (TTI) and is directly correllated to wall tension

and MVO2.

Determinants of MVO2(cont’)

• Increasing systole time (HR) or peak LV systolic pressure

increases the TTI and subsequently MVO2

• Conversely, lowering the AoEDP (decreased afterload)

decreases the pressure the LV must overcome to eject blood

and lowers the TTI

• The Endocardial Viability Ratio relates the relationship

between myocardial O2 supply and demand and is defined by

EVR=DPTI/TTI (supply/demand).

Determinants of Cardiac Output

• CO=SV X HR

• Stroke Volume

*preload (AV synchrony, volume, RV function...)

*afterload

*contractility

• HR

Windkessel Effect• Potential energy stored in aortic root during

systole

• Converted to kinetic energy with elastic recoil of aortic root

• Increases diastolic pressure/flow during early diastole

• Less affect with hypovolemia or noncompliant aortas

• Noted on the A-line tracing as the dicrotic notch.

IABP- how does it work?

• IABP does not ‘pump’ blood per se in contrast to a

VAD.

• Requires a functioning, beating heart.

• IABP serves as an external source of energy to allow

the sick heart to pump more efficiently.

• Does this via afterload reduction and diastolic

augmentation.

• Net result is an increased DO2, decreased MVO2,

and an increased CO.

Concepts of Counterpulsation

• The balloon is phasically pulsed in counterpulsation

to the patient’s cardiac cycle (IABC)

• IABP has no ‘inotropic’ action; does not directly

increase contractility.

• Primarily benefits the left ventricle, although the

diastolic augmentation may improve coronary flow to

both ventricals.

Components

• Double lumen catheter with a distal sausage shaped non-

thrombogenic polyurethane balloon with standard 30-40cc

displacement volumes.

• Pump, equipped with a console display to view the ECG,

aortic and balloon pressure waveforms.

• Central lumen extends to the catheter tip. Serves as a

transducer to measure aortic pressure.

• Central lumen is concentric with and situated inside the helium

channel which is used for balloon inflation.

Placement

• Placed percutaneously or surgically with or without a sheath

via the femoral artery.

• Advanced into aorta under flouroscopy until the tip is about

1cm distal to the origin of the left subclavian a.

• Cathater locations more proximal than this compromise flow

to the vessels of the aortic arch.

• More distal locations attenuate the hemodynamic benefits of

the IABP and can potentially compromise renal blood flow.

Diastolic Augmentation• Balloon inflation at the onset of diastole which is

correllated to aortic valve closure (mechanical event).

• Displacement of blood within the aorta to areas proximal

and distal to the balloon. Termed “compartmentilization”.

• Proximal compartment consists of branches of aortic arch

(carotids) and coronary vasculature.

• Diastolic balloon inflation augments cerebral and coronary

perfusion.

• Increased DPTI and EVR.

• ‘Exaggerated’ Windkessel Effect.

Afterload Reduction• Optimal balloon deflation occurs just prior to the opening

of the aortic valve; during early isovolemic contraction.

• Abruptly decreases intraaortic volume

• AoEDP is acutely decreased (afterload reduction).

• AoV opens sooner during cardiac cycle lending more time

for ventricular ejection

• Overall result is a larger SV (CO).

• A lower peak LVSP decreases the TTI which leads to a

decrease MVO2 and an icrease in the EVR.

Determinants of IABP efficiency

• Ideal balloon volume causes maximal emptying of LV without

causing retrograde flow from the coronary vasculature and

vessels of the aortic arch.

• Balloon should occlude 75-90% of the aortic cross-sectional

area during inflation.

• CO2 vs Helium

• Efficiency if IABC is critically dependent on the timing of

both inflation and deflation.

• Improper timing can worsen a patient’s condition.

IABP Timing

• IABP requires a trigger to determine systole and diastole.

• ECG or arterial waveform.

• ECG directly from the patient to the pump or the pump can

slave off the bedside monitor.

• T-wave default. Electrical index of diastole. Deflation occurs

prior to the next QRS (during PR interval).

• Timing is manually fine-tuned according to the aortic pressure

waveform (more representative of mechanical events).

Arterial Pressure WaveformSYS SYS

DN DN

AVO AVOXDIA DIA

X

ASYS

AUG

sys

DIA

ADIA

DN

Diastolic

Pressure

DicroticNotch

Assisted

SystolicPressure

Systolic

Pressure

Augmentation

Assisted

Diastolic

Pressure

DN DN

Correct Inflation

Just prior to DN

Correct Deflation

ADIA < DIA

ASYS < SYS SYSASYS

ADIA

DIA

Assist Ratios

1:1

1:2

1:4

Early Inflation

• premature closure of aortic valve

– increase in LVEDV and LVEDP

– increased afterload

– increased myocardial oxygen demand

Early Inflation

Early Inflation

Correct Timing

AUG

DN

move inflation

Late Inflation

• sub-optimal coronary perfusion

Late Inflation

Late Inflation

Correct Timing

AUG

DN

move inflation

Early Deflation

• Diastolic augmentation sub-optimal sub-optimal coronary perfusion (potential for retrograde coronary and carotid blood flow)

• sub-optimal afterload reduction increase myocardial oxygen demand.

Early Deflation

move deflation

SYS ASYS

Early Deflation

Correct Timing

Late Deflation

• Afterload reduction almost absentIncreased myocardial oxygen demand due to LV ejecting against a greater resistance and a prolonged isovolumic contraction phase Increased afterload

Late Deflation

move deflation

ADIADIA

Late Deflation

Correct Timing

The Timing Three

Inflation

1. Just prior to dicrotic notch

If > 40ms before – Early Inflation

If dicrotic notch exposed – Late Inflation

The Timing Three

Deflation

1. ADIA < DIA

If ADIA > DIA – Late Deflation

1. ASYS < SYS

If ASYS = SYS – Early Deflation

Limitations of IABC

• Heart Rate

• Arrhythmias (non-sinus rhythms)

• Hypovolemia

Effects of IABP on BP• Normal BP has two reference points- SBP & DBP

• With a pump set at 1:2 you have 5 different reference points.

• Net effect:

*SBP following an augmented beat will be lower than SBP following an unassisted beat.

*AoEDP following an augmented beat will be lower than AoEDP following an unassisted beat.

*Peak diastolic augmented pressure will be integrated into the pressure reading on the arterial line. Overall BP as read by A-line (number you see) should increase.

Weaning

• Frequency ratio weaning (1:1, 1:2, 1:3,

etc.).

• Volume weaning (more physiologic?)

Risk of IABC

• Reported complication rates vary, but in general

range about 20-30% of all IABP’s placed.

• Factors which predispose to a higher complication

rate include age, pre-existing vascular disease,

duration of IABC, DM, HTN, obesity, and

vasopressor therapy.

Complication

Complications

Vasovagal responses due to aortic

stimulation during the

catheterbpassage

Aortic Wall

– Dissection

– Rupture

– Local Vascular Injury

Emboli

– Thrombus

– Plaque

– Air

Complications

IAB Rupture

– Helium Embolus

– Catheter Entrapment

Infection

Obstruction

– Malposition

– Compromised circulation due to catheter

– Ischemia

– Compartment syndrome

Guidelines

“Emergency high risk PCI such as direct PCI for acute MI can

usually be performed without IABP or CPS.

…

However, it should be noted that in patients with borderline

hemodynamics, ongoing ischemia, or cardiogenic shock,

insertion of an intra-aortic balloon just prior to coronary

instrumentation has been associated with improved outcomes.

Furthermore it is reasonable to obtain vascular access in the

contralateral femoral artery prior to the procedure in patients

in whom the risk of hemodynamic compromise is high…”

AHA/ACC Guidelines for PCI, Circulation 2005

Summary • Intra-Aortic Balloon Pump is an excellent tool for the

management of hemodynamically unstable patients especially in the setting of acute MI

• Understanding the Cardiac Physiology is important (determinants of myocardial O2 delivery, O2 consumption, cardiac output and Windkessel effect)

• Timing of IABP will influence the outcome

• IABP therapy will remain the mainstay of temporary mechanical cardiovascular support for years ahead.