Pacemakers and IABP Air Evac EMS Patient Care Services Internship Program 5 th Month Module 4 Proprietary property of Air Evac EMS Inc

Pacemakers and IABP

Air Evac EMS

Patient Care Services

Internship Program

5th Month Module 4

Proprietary property of Air Evac EMS Inc.

Objectives

• Review cardiac anatomy and physiology as it pertains to hemodynamics and critical care monitoring.

• Review principles of cardiac function that are required for hemodynamic stability


Terminology Review

• Cardiac Output

• Preload

• Afterload

• Contractility

• Stroke Volume

• MVO2

Physiology of the Heart


• CO (Cardiac Output) = Stroke volume X HR– Normal CO for adult is 4-8 L/min.– Heart rate– Stroke Volume

• is the amount of blood forced out of the ventricle with each contraction

• Normal Stroke volume is 50-100cc per beat• Stroke volume is effected by contractility, afterload

and preload



Hemodynamic Basics


Preload ◦ Amount of stretch in the heart muscle just before

contraction◦ Is fluid dependant

Afterload◦ The force that must be overcome by the left ventricle to

eject blood◦ Dependant on aortic valve, aortic end diastolic pressure

and vascular resistanceMVO2

◦ Myocardial oxygen demand.◦ Largest part of MVO2 is used to overcome afterload◦ The greater the impedance to blood flow (afterload), the

greater the MVO2



• Contractility– Strength of contraction of the heart muscle– Starling’s Law– Electrolyte’s are important players in

contractility.• K+, C++, catecholamines

– We can give inotropes to increase contractility– Contractility can be reduced to a point to where

the body and the heart itself is not receiving adequate blood and oxygen



Adrenergic Receptors and CV effects of stimulation


Heart Rate

• Increased – SNS Stimulation

• Decreased– PNS Stimulation– Conduction disorders

• Treatments to Increase– Sympathomimetics– Parasympatholytics– Pacemaker

• Treatments to Decrease– Cardiac glycosides– Beta Blockers– Ca Channel blockers– Vagal maneuvers– Cardioversion


Afterload• Increased

– Vasoconstriction (SNS mediated or pharmacologic)– HTN– Pulmonary HTN– Valvular disease (aortic)

• Decreased– Hypotension– Vasodilation (Shock)

• Treatments to Increase– Vasopressors

• Treatments to Decrease– Arterial vasodilators– ACE inhibitors– IABP


Preload• Increased

– Heart Failure– Hypervolemia– Brady-dysrhythmias

• Decreased– Hypovolemia– Excessive vasodilation– Increased intrathoracic pressure (PPV)– Tachydysrhythmias

• Treatments to Increase– Isotonic fluids– Colloids– Blood/ Blood Products

• Treatments to Decrease– Diuretics– Vasodilators– ACE inhibitors


Contractility

• Increased– SNS Stimulation– Sympathomimetic drugs

• Decreased– MI– Cardiomyopathy– Hypoxemia– Acidosis

• Treatments to Increase– Cardiac glycosides– Sympathomimetics

• Treatments to Decrease– Beta Blockers– Ca Channel blockers



Pacemakers

• An electronic device that delivers an electrical stimulus to the heart to depolarize the myocardium and increase or decrease the heart rate.

• Indications:– Sick sinus syndrome– Refractory tachydysrhythmias– Bi-fasicular or Tri-fasicular block/ AV Blocks


Sick Sinus Syndrome

• Symptomatic sinus arrest

• Suppression of ventricular ectopy resulting from bradycardia

• Atrial fibrillation

• Brady-tachy syndrome

• Symptomatic sinus bradycardia


Heart Blocks

• Type I and type II second degree AV blocks

• Acute bifascicular or trifascicular block

• Complete AV block

• Sinus arrest with ventricular asystole


Drug Refractory Dysrhythmias

• Overdrive ventricular pacing to suppress or prevent ventricular ectopic activity

• Overdrive atrial pacing to break supraventricular tachycardia or atrial flutter


Cardiovascular Surgery

• Prophylactic use during anesthesia and surgery in patients with a history or acute coronary syndrome or cardiac dysrhythmias

• Treatment for complete heart block developed during or after surgery

• Cardiac output augmentation postoperatively


Types of Pacemakers

• Temporary (External Pulse Generator)– Transthoracic Epicardial

• Electrodes attached to epicardium of atrium, ventricle or both during cardiac surgery & brought thru the chest wall.

– Transcutaneous Endocardial• Pacing leads inserted percutaneously via IJ or SC vein and advanced in to the RA/ RV

or both.

– Transcutaneous (noninvasive)• Percutaneous leads applied to chest and back-used during codes until transvenous

pacer can be inserted.

• Permanent– Transvenous endocardial

• Lead inserted in the cephalic vein advanced into the RA or RV-pulse generator implanted in SC fat under the clavicle

– Epicardial • Electrodes sewn onto epicardium; pulse generator implanted in SC fat of the abdomen.

– Removal can cause tamponade to occur


Types of Pacemakers

• Asynchronous– Fixed rate– Delivers a pacing stimulus at a fixed rate regardless

of the heart’s intrinsic activity– Rarely used these days

• Synchronous– Demand pacing– Delivers a pacing stimulus only when the heart’s

intrinsic pacemaker fails to function at a predetermined rate.

– Stimulus can be triggered or inhibited when the intrinsic activity is seen.


Concepts of Pacemaker Function

• Connectivity– Unipolar wires

• A single negative electrode placed in the chamber being paced

– Bipolar wires• Negative and Positive electrodes placed in the chamber

being paced

• Output• Capture• Sensitivity


Output

• Three components:– Rate– Amount– Chamber

• Rate is dependent upon the needs of the patient• Amount is the amount of energy delivered by the pulse

generator to the heart to initiate depolarization• Chamber

– Atrial (A)– Ventricular (V)– Both (D)


Output Failure


Capture

• The ability of the electrical impulse to initiate a cardiac response

• Indicated by a pacer spike followed by a corresponding P wave or QRS complex

• Electrical capture-electric impulse

• Mechanical capture-pulse associated with the electrical impulse


Sensitivity

• A function of the pacemaker to interpret electrical signals for the initiation or inhibition of a response by the pacemaker.

• Factors that affect the ability of a waveform to be sensed:– Voltage– Amplitude– Pulse width– Frequency


Failure to Sense


Pacing & Electrophysiology Codes

• Chamber of Stimulation– Atrial: AAO, AAI

• Pacing stimulus occurs before the P wave• MUST have an intact AV node

– Ventricular: VOO, VAT, VVI, VVT, VDD• Pacing stimulus occurs before the QRS complex

– Atrioventricular (AV) sequential: DOO, DVI, DDD• Maintains benefit of atrial kick (CO)• Pacing stimulus is before both or either P-wave or QRS

complex• Allows for complete ventricular filling


Pacing & Electrophysiology Codes

• Rate responsive: AAIR, VVIR, DDDR– Heart rate is adjusted according to demands

for cardiac output• Heart rate changes are stimulated by changes in

muscle activity, minute ventilation or changes in blood temperature or pH.


Pacing Problems

• Failure to capture– Always make sure you have a pulse with electrical activity– Visible spike with no P wave or QRS complex

• Over sensing– Pulse generator senses events that are inappropriate or non-cardiac in

origin

• Under sensing– Failure to sense intrinsic cardiac signals– Emits inappropriately timed, asynchronous or competitive output pulses

• Pacing rate changes• Output failure


Ventricular Pacing


Atrial Pacing


AV Sequential Pacing


Medtronic 5348

Rate setting. Settings from 30-180

Milliamp setting. Settings from 0.1-20 mA

Sensitivity setting. Asynchronous to most synchronous

Power buttons and standard 9 volt battery compartment

Intra-aortic Balloon Pump

Concepts and Physiologic Principles of IABP


• Anatomy of the heart and great vessels• Physiology of the cardiac cycle• Concept and physiologic principals of IABP• Indications for IABP• Contraindication for IABP• Insertion, timing, and waveforms• Assessment, management and troubleshooting

Objectives


Anatomy of the Heart

Important points:◦ Left and right heart chambers

Remember the ventricles do the “pumping” and are responsible for overcoming afterload

◦ 4 valves Tricuspid, pulmonary, mitral and aortic The aortic valve is where

blood exits from the left ventricle when blood is pumped to the periphery


Important Points:• The coronary arteries begin at the

root of the aorta just behind the

aortic valve

• The coronary arteries are

embedded in the myocardium and

thus little flow occurs during systole

• The opened aortic valve also partially covers the opening to the coronary arteries during systole

• The majority of blood flow to the coronary arteries happens during diastole

Anatomy of the Heart


The weakened heart

• Ischemia and acidosis have a negative effect on contractility

• Damaged myocardium from MI– Increased work load on remaining myocardium– Coronary perfusion can’t keep up with demand– Individuals whose heart muscle builds up overtime and “dilate”, do

so to a certain point then lose the “Starling effect” and lose some contractility (e.g. dilated cardiomyopathy)

– LV function is diminished which means the heart is not able to “eject” as much blood as it used to or it takes more effort to do so


The weakened heart

An MI and the three types of cardiomyopathy are examples of the heart muscle being weakened or not being able to provide the work as it did beforeProprietary property of Air Evac

EMS Inc.

Indications for use:◦ IABP is used for a “sick” failing heart◦ Cardiogenic shock after MI◦ Complications from MI such as post-infarction VSD,

mitral regurgitation and papillary muscle rupture◦ Bridge to cardiac transplantation◦ Acute LV failure after cardiac surgery◦ Weaning from cardio-pulmonary bypass◦ Sepsis◦ Used in larger hospitals for general surgeries on

patients who would have been “too sick” to operate on otherwise

Concepts and Physiology of IABP


A Little HistoryThe IABP was pioneered in the 1960’s.The first IABP was used during a heart surgery in 1976 and has since become more widely used.

Early model IABPProprietary property of Air Evac

EMS Inc.

• Anyone who has had the privilege of transporting one of the original IABP’s knows that they are now much smaller and more compact which makes for easier transport

• IABP has been made “smarter” by manufacturers which benefits both patient and operator

A Little History


IABP-How does it work?

•A long slender balloon on the end of a catheter is inserted through a sheath into the femoral artery

•Inserted percutaneously most of the time, ideally through a sheath left from a cardiac catheterization

•Transthoracic insertion is less common and may be used emergently during open heart surgery or if there is contraindications to using the patients femoral arteries as an insertion site

•Complications of insertion include bleeding, air embolism and laceration of the artery to name a few


The balloon is inserted into the thoracic aorta just distal to the take-off of the left subclavian artery

It is placed proximal to the renal arteries

There is a pressure sensor on the tip of the catheter

Note: the importance of proper placement (renal arteries and L SC)

How does it work?


• The IABP has a base unit which inflates and deflates the balloon in synchronization with the cardiac cycle

How does it work?


• Rapid inflation and deflation of the balloon in synchronization with the cardiac cycle

• The balloon inflates with helium which has a low molecular weight and flows and fills easier and faster than other gases

• Amount of helium inflating balloon depends on the size of the balloon

• The balloon inflates during diastole and deflates immediately before systole

How does it work?


Inflation occurs during diastole Increases:

Aortic root pressure Aortic diastolic pressure CPP O2 supply (MVO2) Stroke volume

When the balloon is inflated blood is pushedback against the closed aortic valve increasing coronary artery perfusion

Another important concept is that theaorta actually expands and contracts

How does it work?


• Deflation occurs immediately prior to systole

• Decreases:– Aortic end-diastolic pressure

– Impedance to ejection

– Afterload

– Oxygen demand (MVO2).

• Timing of deflation is important because you wouldn’t want an already sick heart trying to eject blood against an inflated balloon

How does it work?


• Timing of the inflation and deflation of the balloon is extremely important

• The first IABP’s had to be adjusted manually for timing– This conventional method left the timing up to

the operator– Because of timing and sensing, the first

IABP’s didn’t function adequately with arrhythmia's or tachycardias

IABP Timing


IABP Timing-Inflation

Manual timing of the IABP is based on aortic pressure waveforms and EKG tracings

The dicrotic notch is usedto determine inflation time

The dicrotic notch represents closure ofthe aortic valve on a pressure waveform

Think about this:◦ You wouldn’t want the

balloon inflating with theaortic valve still open


Deflation occurs immediately before systoleMethods used for deflation timing

◦ This was originally set by the operator◦ R wave on ECG for deflation◦ If the patient is paced, the pacer spike may be used for deflation

trigger. (A or V pacing)The newest modern day IABP’s have auto-timingNew technology

◦ Smaller equipment◦ Use of fiberoptic’s and computer based physiology

based timing algorithms that operate reliably in arrhythmia’s

IABP Timing-Deflation


Inflation occurs at the dicrotic notch

“R” wave used for deflation


Important Notes:◦ With new technology timing has become automated◦ Remember than inflation and deflation can be

“triggered” off of EKG tracings, pressure tracings, pacer spikes and a “demand” time interval

◦ These “triggers” are what causes the IABP to start and end cycles

◦ Some sense changes from beat to beat and adjust accordingly

◦ Triggers are set according to heart rhythm and should be used according to manufactures recommendations Consideration – loss of pulsatile flow in bypass patients

IABP Timing


Correct Timing• Inflation has occurred at the

dicrotic notch

• Inflation of the balloon has caused increased coronary artery perfusion and increased MVO2 and is reflected by diastolic augmentation

• Deflation has occurred and reduced the impedance to ejection

• Afterload is reduced• MVO2 is decreased• Reflected by the assisted aortic

end-diastolic pressure

IABP Timing Early inflation

◦ Diastolic augmentation encroaches onto systole

◦ Inflation has been initiated prior to dicrotic notch

◦ Increase in intra-aortic pressure while aortic valve is still open

◦ Can cause increase SVO2 demand

◦ Can cause premature closure of AV valve

◦ Aortic regurgitation◦ Potentially harmful timing error


• Late inflation– Inflation after the dicrotic notch– Sub-optimal coronary artery

perfusion– Minimal displacement of blood

for augmentation– Potential timing problems

with next systole

IABP Timing


• Early Deflation– Deflation occurs before systole– The “vacuum” effect and

afterload reduction is lost

IABP Timing


• Late Deflation

– Deflation occurs after systole has begun

– Increases afterload– Increase LV workload– Increases SVO2– Very harmful to the

patient

IABP Timing


• Most IABP’s can be set to 1:1, 1:2, 1:3 ratios– One pump or balloon assist for every heart beat or for

every other, etc– When manually adjusting timing IABP must be in 1:2

assist ratio

• Physician may go from 1:1 to 1:2 or 1:3 for “weaning”

• Must have good EKG waveforms and good pressure tracings to operate properly

IABP Timing

Insertion◦ Percutaneous insertion with or without a sheath most

of the time in the femoral artery◦ Different sizes of balloons◦ Complications

Bleeding at site Laceration of artery

◦ “Autofill” or manual fill of balloon before initiation of pump

◦ CXR to confirm balloon placement Radiopaque tip at 2nd to 3rd ICS

◦ “Mark” depth of insertion of catheter

Clinical Considerations


• Contraindications– Aortic insufficiency– Severe aortic disease– Severe peripheral vascular disease– Conduit or graft of femoral artery



• Adequate hydration is important

• Labs– H & H, PT, PTT, PLT, WBC’s– UO– All very important.– The mechanical pumping of the IABP can cause

thrombocytopenia and can change blood count and clotting levels quickly

• May see prophylactic broad spectrum antibiotics given if IABP in for more than 48 hours



• The central aortic pressure is monitored using a transducer and pressure tubing set up

• The IABP transducer must be routinely “zeroed” as with any pressure line– Knowledge in pressure waveforms– Knowledge of catheter kink, catheter whip, etc.

• Depending on physician, you may see heparin added to pressure bag



Limb ischemia◦ Assess and document Q15◦ Assess pedal pulses often◦ Asses temperature and color in feet and toes often◦ Treatment involves removal of IABP (NOT by you)◦ Compartment syndrome after removal

Bleeding◦ Check labs◦ Direct pressure◦ May need blood products◦ Is heparin being used in the pressure bag?◦ Assess “site” often◦ Watch for any blood in the pneumatic tubing

Aortic Dissection◦ Pain between should blades.◦ Drop in BP◦ Loss of pedal pulses

Complications


• Balloon leak– Blood in pneumatic tubing– Low augmentation pressure– Gas loss alarm– IAB catheter alarm– Will result in discontinuation of IAB

Complications


Immobilize legSecure catheterMeasure depth of insertionDo not raise HOB above 30 degreesExtra helium tankPower SupplyLarge 60cc syringe and stop cock

◦ IAB should not remain immobile for greater than 30 minutes because of possibility of clot formation. Manual pumping with syringe per manufacturers recommendations (3-5 minutes).

Important Transport Considerations


Urine Output◦ An acute decrease in UO can mean the balloon has

migrated down and is blocking the renal arteriesDistal pulses

◦ Migration of balloon up and blocking left SC artery IABP console will “purge” occasionally, and will do so

with altitude changes during transportDoppler for assessment of weak distal pulsesGCSMonitoring of PA, CVP and wedge pressuresSedation/pain controlAcceptable hemodynamic parameters

Important Transport Considerations


• In Closing– Knowledge, training and familiarization of the

IABP that you use is paramount– Frequent assessment of the patient and the

pump



Documents

Pacemakers and IABP Air Evac EMS Patient Care Services Internship Program 5 th Month Module 4 Proprietary property of Air Evac EMS Inc