Week 7 Hemodynamics Flashcards
Hemodynamics is
The study of the motion of blood through the body.
Fundamental Concepts of hemodynamics
Cardiac Output
Preload
Afterload
Contractility
Normal Hemodynamic Values SVO2
60-75%
Normal Hemodynamic Values Stroke Volume
50-100ML
Normal Hemodynamic Values Stroke Index
25-45mL/M2
Normal Hemodynamic Values Cardiac Output
4-8 L/min
Normal Hemodynamic Values MAP
60-100mm Hg
Normal Hemodynamic Values CVP
1-7mm Hg
Normal Hemodynamic Values PAP systolic
20-30mm Hg
Normal Hemodynamic Values PAP Diastolic
5-15 mm Hg
Normal Hemodynamic Values PAOP (wedge)
8-12 mm Hg
Normal Hemodynamic Values SVR
900-1300 dynes.sec.com
Cardiac Output
The cardiac output pushes the blood through the vascular system.
Cardiac output (CO) is calculated by multiplying the heart rate (HR) by the stroke volume (SV).
Stroke volume is the volume of blood pumped out of the heart with each heartbeat.
If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output.
This is known as compensatory tachycardia.
heart rates greater than 150 bpm actually drop stroke volume
Cardiac Index =
CO/BSA=2.4 - 4.0L/min/m2
BSA = height in c weight in k divide by 360 then divide all that by 2
Stroke volume is affected by three factors:
preload, afterload, and contractility
Compensatory tachycardia
If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output.
Preload
the amount of stretch on the cardiac myofibril at the end of diastole.
When the ventricle is at its fullest
Preload is most directly related to:
Fluid volume
Starling’s curve:
describes the relationship of preload to cardiac output As preload (fluid volume) increases, cardiac output will also increase until the cardiac output levels off. If additional fluid is added after this point, cardiac output begins to fall.
Preload Measurement
Not measured directly…instead measured by physical assessment of fluid volume
Signs of inadequate preload include:
Poor skin turgor Dry mucous membranes Low urine output Tachycardia Thirst Weak pulses Flat neck
Signs of excess preload in a patient with:
distended neck veins
crackles in the lungs
Bounding pulses
Increased preload in a patient with poor cardiac function presents with
crackles in the lungs S3 heart sound, low urine output Tachycardia cold clammy skin with weak pulses edema
Preload
Insufficient preload is commonly called hypovolemia or dehydration.
Insufficient volume is present in the vascular tree, the sympathetic nervous system is stimulated to release the atecholamines, epinephrine and norepinephrine.
These hormones cause increased heart rate and arterial vasoconstriction.
The increased heart rate produces a compensatory tachycardia while the vasoconstriction helps maintain an adequate blood pressure.
If these patients are treated with catecholamine drugs rather than receiving volume infusions, the tachycardia becomes very pronounced and the vasoconstriction can become severe enough that the organs fail and the distal extremities become ischemic.
The first step in treating any form of hemodynamic instability is:
to assess the patient for signs of insufficient preload (e g volume or blood loss)
Afterload is:
the resistance that the ventricle must overcome to eject its volume of blood.
The most important determinant of afterload is
vascular resistance
Other factors affecting afterload include:
blood viscosity
aortic compliance
valvular disease.
As arterial vessels constrict, what happens to afterload?
the afterload increases
As arterial vessels dilate, what happens to afterload?
the afterload decreases
Increased CO
higher volumes
Decreased CO
decreased volumes
In general, when you have someone with signs of low preload treat with
volume, until you know if its a stretch issue
High Afterload:
increases myocardial work and decreases stroke volume.
Patients with high afterload present with signs and symptoms of arterial vasoconstriction including
cool clammy skin
capillary refill greater than 5 seconds
narrow pulse pressure.
Pulse pressure is calculated by:
subtracting the diastolic blood pressure (DBP) from the systolic blood pressure (SBP).
What is normal pulse pressure at the brachial artery
40 mm Hg
Low afterload:
myocardial work and results in increased stroke volume.
Patients with low afterload present with symptoms of arterial dilation
warm flushed skin
Bounding pulses
wide pulse pressure
If the afterload is too low, what may result?
hypotension
Points to ponder for afterload:
A key component of treatment for heart failure is afterload reduction using beta-blockers and ACE inhibitors.
By decreasing the resistance to ventricular ejection the cardiac output is increased and myocardial workload is decreased.
The increase in cardiac output frequently improves the functional status of these patients.
ACE inhibitors
Beta blockers
Contractility refers to
the inherent ability of the cardiac muscle to contract regardless of preload or afterload status.
Contractility is enhanced by
exercise, catecholamines, and positive inotropic drugs.
Contractility is decreased by
by hypothermia, hypoxemia, acidosis, and negative inotropic drugs.
Myocardial compliance refers to
the ventricle’s ability to stretch to receive a given volume of blood.
Normally the ventricle is very compliant so large changes in volume will produce small changes in pressure.
If compliance is low, small changes in volume will result in large changes in pressure within the ventricle.
If the ventricle cannot stretch, it will be unable to increase cardiac output with increased preload.
Tissue perfusion is the
transfer of oxygen and nutrients from the blood to the tissues.
When performing interventions designed to improve hemodynamics
valuation of effectivess is whether or not the intervention was successful in improving tissue perfusion.
Many of the signs of inadequate preload, afterload and contractility also reflect poor tissue perfusion.
Cool clammy skin Cyanosis Low urine output Decreased level of consciousness Metabolic acidosis Tachycardia Tachypnea Hypoxemia
Labs and diagnostic testing that are used to evaluate tissue perfusion include
Arterial blood gases
Arterial lactate levels
Pulse oximetry.
Poor tissue perfusion is reflected by a low pH, low base excess and elevated lactate level.
Pulse oximetry readings are typically low when tissue perfusion is compromised to a significant degree.
Methods of Hemodynamic Monitoring
Arterial Blood Pressure Central Venous Pressure/ Right Atrial Pressure The Pulmonary Artery Catheter Cardiac Output Measurement Tissue Oxygenation
Arterial Blood Pressure
Non-invasive
MAP most accurate
Direct arterial pressure measurement
Reasons for Hemodynamic Monitoring
Assessment of cardiovascular function (complicated MI, Cardiogenic shock, papillary muscle rupture)
Peri-operative monitoring of surgical patients with major systems dysfunction
Shock of all type (septic, hypovolemic, any shock that is prolonged or origin is unknown)
Assessment of pulmonary status
Assessment of fluid status (dehydration, hemorrhage, GI bleed, burns)
Therapeutic indications (cardiac pacing )
Diagnostic indications (pulmonary hypertension)
Arterial Blood Pressure Site Selection; The most preferred insertion site
is the radial artery
alternate Arterial blood pressure sites include
the femoral and brachial arteries.
The femoral artery is not a preferred site due to its anatomic location.
if the radial artery is used
Assess site with modified Allen test
performed prior to cannulation to ensure that the ulnar artery provides adequate circulation to the hand to prevent tissue ischemia or necrosis.
Indications for Arterial Catheterization Need for continuous blood pressure measurement
Hemodynamic instability
Vasopressor requirement
MAP should be 60-100mm/Hg
Indications for arterial catheterization Respiratory failure
Frequent arterial blood gas assessments
Indications for Arterial Catheterization most common locations
radial, femoral, axillary, and dorsalis pedis
What size is the art line catheter
The intra-arterial catheter is typically a 20-gauge intravenous-type catheter
What is important about the art line transducer?
must be level with the art line insertion site!!! If not you will get false readings
Obtaining Blood Draws from the A-Line
Using proper technique when obtaining blood from an intra-arterial catheter:
Maintain aseptic technique for any line access and use standard precautions
Withdraw blood gently and slowly from the line
Waste the first 5mL
Flush the collection port to prevent clot formation and bacterial colonization
Maintain sterility of the system; place a new sterile cap over the sample port
Fast-flush the system to the patient for no more than 3 seconds at a time
Do not use a syringe to manually flush arterial catheters
Manual flushing with a syringe generates enough pressure that the injected fluid can invade the cerebral circulation
Complications of Arterial Catheterization
Hemorrhage Hematoma Thrombosis Proximal or distal embolization Pseudoaneurysm Infection
Limitations of Arterial Catheterization
Pressure does not accurately reflect flow when vascular impedance is abnormal
Systolic pressure amplification
Mean pressure is more accurate
Recording artifacts
Underdamping
Overdamping
Central Venous Catheterization:Central venous pressure
Right atrial (superior vena cava) pressure
Limited by respiratory variation and PEEP
Central Venous Catheterization: Central venous oxygen saturation
SCVO2
Correlates with SMVO2 assuming stable cardiac function
Central Venous Pressure Waveform: The central venous catheter
may be a large or small-bore catheter with one or more lumens inserted via the subclavian, internal jugular or external jugular vein.
Right Atrial Pressure Monitoring Indications
Measure right atrial pressure (RAP)
Same as Central Venous Pressure (CVP)
1-7 mm Hg
Assess blood volume; reflects preload to the right side of the heart
Assess right ventricular function
Infusion site for large fluid volume
Infusion site for hypertonic solutions
Reasons for elevated CVP/ RA pressure:
decreased right (or single) ventricle compliance tricuspid valve disease Intravascular volume overload cardiac tamponade tachyarrhythmia
Reasons for reduced RA pressure:
low intravascular volume status
inadequate preload
Right Atrial Pressure Monitoring Waveform Analysis
a wave:
rise in pressure due to atrial contraction
Right Atrial Pressure Monitoring Waveform Analysis
c wave
rise in pressure due to ventricular contraction and closure of the tricuspid valve
Right Atrial Pressure Monitoring Waveform Analysis
x decent
fall in pressure due to atrial relaxation increase in atrial pressure
Right Atrial Pressure Monitoring Waveform Analysis
v wave
rise in pressure during atrial filling
passive filling
Right Atrial Pressure Monitoring Waveform Analysis
y decent
all in pressure due to opening of the tricuspid valve and onset of ventricular filling(passive)
Right Atrial Pressure Monitoring Waveform Analysis
Elevated RAP
RV failure Tricuspid regurgitation Tricuspid stenosis Pulmonary hypertension Hypervolemia Cardiac tamponade Chronic LV failure Ventricular Septal Defect Constrictive pericarditis
Right Atrial Pressure Monitoring Waveform Analysis
Decreased RAP
Hypovolemia
Increased contractility
The Pulmonary Artery Catheter
Widespread use in critically ill patients
Remains controversial
The Pulmonary Artery Catheter measures
CVP PAP PAOP Cardiac Index SVO2
How many PACs are inserted annually?
approximately 1 million
Components of a Pulmonary Artery Catheter (PAC or Swan Ganz) The pulmonary artery catheter normally has four ports which include:
The proximal port which is used for central venous pressure monitoring
The distal port which measures pulmonary artery and pulmonary artery wedge pressure
The balloon port with 1.5ml special syringe for measurement of pulmonary artery wedge pressure
The thermistor connector to assist with cardiac output measurement
Nursing Responsibilities Pre-Insertion PAC
Explain procedure to patient
Assemble all equipment
Set up all monitoring lines aseptically
Prime all IV tubing and transducer flush lines (Pressure Bag @ 300 mmHg)
Connect PAC cable to monitor and attach to transducer
Connect CVP cable to monitor and attach to transducer
Check PAC packaging for to ensure sterility/expiration date
Zero transducers (mid axillary)
Place monitor in wedge/insertion mode (scale should be 30-60)
Turn on and set continuous cardiac monitor/Svo2 monitor for insertion (make sure previous patient data is erased)
Nursing Responsibilities During Insertion PAC
Position patient for insertion (flat for femoral, Trendelenburg for subclavian or jugular)
Assist with creating a sterile field
With the assistance of the physician, open PAC and connect transducers to the distal and proximal lumens
Connect the IV line to the medication port
Connect the cardiac output cable and Svo2 cables
Remove the 1.5 ml syringe and connect it to the syringe port
Zero catheter while still in package
Inflate air into the balloon to assure balloon integrity prior to insertion
After physician places sterile sheath over catheter, waveform presents should be assessed on the monitor (usually a small shake of the catheter itself will confirm)
Once physician inserts and advances the catheter to right atrium, he will request that the RN inflate the balloon
If for any reason during floatation of a PAC the physician wishes to withdraw the catheter, the balloon must be deflated
During floatation of a PAC the right atrial (CVP), right ventricle, pulmonary artery and pulmonary artery wedge pressure (PAWP) waveforms/pressure tracings should be noted and printed
Nursing Responsibilities Post-Insertion PAC
Make sure that PAC cap is in the lock position so catheter will not migrate
Secure catheter to patient with tape
Apply occlusive dressing
Set high and low alarms on monitor as appropriate for patient
Double check to assure that physician has disposed of all sharps
Double check to see that Chest X-ray was ordered
Nursing Documentation Post-Insertion PAC
Vital signs, pulmonary artery pressures, Svo2 saturation (immediately after insertion and per standard)
PAC insertion site and how far it was advanced (in cm)
Amount of air required to inflate balloon to obtain PAWP pressure
Verification of X-ray placement of PAC
Print and place waveform strips on nursing flow sheet
Patient tolerance of procedure
Medications given during procedure
Nursing Responsibilities For Removal
Make sure the balloon is COMPLETELY deflated. Pull back extra, then lock.
When removing, if piece of catheter is left in patient, IMMEDIATELY put patient in trendelenburg and place pt on left side.
Increased Systolic Pulmonary Artery Pressure Caused by any of the following:
Any Factor that increases PVR Pulmonary Embolism Hypoxemia COPD ARDS Sepsis Shock Primary Pulmonary Hypertension Restrictive Cardiomyopathy Significant left-to-right shunting
Increased Diastolic Pulmonary Artery Pressure Caused by any of the following
Any Factor that increases pulmonary artery systolic pressure Intravascular volume overload Left Heart Dysfunction Mitral Stenosis/Regurgitation Aortic Stenosis/Regurgitation Decreased LV Compliance Cardiac Tamponade/Effusion
Pulmonary Artery Systolic and Diastolic Pressure Decreased
Hypovolemia
Severe Tricuspid or Pulmonic Stenosis
Changes in PAWP Increased
Left Heart Dysfunction Mitral Stenosis/Regurgitation Aortic Stenosis/Regurgitation Decreased Left Ventricular Compliance Intravascular Volume Overload Tamponade/Effusion Obstructive Left Atrial Myxoma Restrictive Cardiomyopathy
Changes in PAWP Decreases
Hypovolemia
Pulmonary Embolism
Complications of Pulmonary Artery Catheterization: General central line complications
Pneumothorax
Arterial injury
Infection
Embolization
Other Complications of Pulmonary Artery Catheterization:
Inability to place PAC into PA
Arrhythmias (heart block)
Pulmonary artery rupture
Contraindications…when would you not want to place a PAC
Tricuspid or pulmonary valve mechanical prosthesis
Right heart mass (thrombus and/or tumor)
Tricuspid or pulmonary valve endocarditis
Atherosclerotic heart disease without heart failure
Angioplasty or other interventional procedures
Thermodilution Method of Cardiac Output Measurement
Measuring Cardiac Output
Inject fluid in to r atrium, fluid migrates through, change in temp over time and tells you how well the heart is contracting
Tissue Oxygenation
Despite advances, our ability to monitor the microcirculation and tissue perfusion is limited
Laboratory tests for metabolic acidosis are global and insensitive
Newer technology
Gastric tonometry reads the co2 in the stomach, helps determine acidotic state
Sublingual capnometry
Nursing HOURLY assessment:
Air in line or stopcocks Precipitates Leaking at site Increasing resistance Condition of entrance sites
Equipment Used in Hemodynamic Monitoring:Semi-rigid pressure tubing
attaches the catheter to a transducer set-up.
The tubing must be more rigid than standard IV tubing so that the pressure of the fluid within it does not distort the tubing.
If the tubing is distorted in this way, the pressure readings will be inaccurate.
The tubing must also be as short as reasonably possible.
Longer tubing will cause distortion of the pressure as it travels over the longer distance.
Equipment Used in Hemodynamic Monitoring: transducer
a device that converts the pressure waves generated by vascular blood flow into electrical signals that can be displayed on electronic monitoring equipment.
Equipment Used in Hemodynamic Monitoring: transducer cable
attaches the transducer to the monitor, which displays a pressure waveform and numeric readout.
Equipment Used in Hemodynamic Monitoring: flush system
consists of a pressurized bag of normal saline (which may or may not contain added heparin, depending on the unit and facility where you work).
The pressure must be maintained at 300 mm Hg to prevent blood from the arterial system from backing up into the pressure tubing.
Equipment Used in Hemodynamic Monitoring: intraflow valve
part of the transducer setup and maintains a continuous flow of flush solution (approximately 3-5 ml/hr) into the monitoring system to prevent clotting at the catheter tip.
Equipment Used in Hemodynamic Monitoring: fast flush device
allows for general flushing of the system and rapid flushing following withdrawal of blood from the system or when performing a square wave test.
Transducer Leveling: phlebostatic axis
located at the 4th intercostal space, halfway between the anterior and posterior chest (mid-chest).
Derived Pressures
Cardiac Index (CI)
Stroke Volume (SV) – CO/HR
Stroke Volume Index (SVI) – CI/HR
MAP- SBP + 2(DBP)/3
Systemic Vascular Resistance (SVR)- (MAP-RAP) x 80/CO
Systemic Vascular Resistance Index (SVRI) - (MAP-RAP) X80/CI
Hemodynamic Emergencies: LV Failure
HR ↑ MAP CO CVP/RAP PAP/PAWP Notes
Hemodynamic Emergencies: Pulmonary Embolism
HR ↑ MAP CO CVP/RAP PAP/PAWP Notes
Hemodynamic Emergencies: Cardiogenic pulmonary edema
HR ↑ MAP CO CVP/RAP PAP/PAWP Notes
Hemodynamic Emergencies: cardiac tamponade
HR ↑ MAP CO CVP/RAP PAP/PAWP Notes
Hemodynamic Emergencies : RV Failure
HR ↑ or varies MAP CO CVP/RAP PAP/PAWP Notes
Hemodynamic Emergencies : Cardiogenic Shock
HR ↑ MAP CO CVP/RAP PAP/PAWP Notes
Hemodynamic Emergencies : Septic Shock
HR ↑ MAP CO CVP/RAP PAP/PAWP Notes
Hemodynamic Emergencies: Hypovolemic Shock
HR ↑ MAP CO CVP/RAP PAP/PAWP Notes
Vasopressors/Inotropes
Dopamine Dobutamine Epinephrine Phenylephrine Norepinephrine Vasopressin
Dopamine
Dose dependent receptor activation
Low dose (1-5mics) - increases blood flow via dopamine receptors in renal, mesenteric, cerebral circulation
Intermediate dose (5-10mics) - increases cardiac output via - receptors
High dose(>10mics) - progressive vasoconstriction via -receptors in systemic and pulmonary circulation
In vivo, receptor effects are often mixed
Tachyarrhythmias are most common complication
Low dose dopamine has no proven renal benefit
Significant immunosuppressive effects through suppression of prolactin from hypothalamus
Dobutamine
Synthetic catecholamine generally considered the drug of choice for severe systolic heart failure
Increases cardiac output via Beta 1 -receptor and causes vasodilation via Beta 2 -receptor
Inotropic and chronotropic effects are highly variable in critically ill patients
Data supports use in septic shock when cardiac output remains low despite volume resuscitation and vasopressor support
Epinephrine
The most potent adrenergic agent available
Potency and high risk of adverse effects limit use to cardiac arrest (and specific situations after cardiac surgery)
Primarily Beta receptor effects at low doses and alpha receptor effects at high doses
Arrhythmogenic
Phenylephrine
Relatively pure beta adrenergic agonist
Minimal inotropic effects; often causes reflex bradycardia
Consistently decreases cardiac output
Increased propensity to cause ischemic complications
Be wary in the OR
Norepinephrine
More potent vasoconstrictor than dopamine; some inotropic effect
Potent alpha 1 stimulation
Moderate beta 1 activity
Minimal beta 2 activity
Vasopressin
Acts on vascular smooth muscle via V1 receptors, independent of adrenergic receptors
Considered replacement therapy
Traditionally not titrated
Significant splanchnic vasoconstriction
Intra-Aortic Balloon Pump (IABP)
The Intra-Aortic Balloon Pump (IABP) is a circulatory assist device that is used to support the left ventricle.
Principles of the IABP
A flexibile catheter is inserted into the femoral artery and passed into the descending aorta.
Correct positioning is critical in order to avoid blocking off the subclavian, carotid, or renal arteries.
When inflated, the balloon blocks 85-90% of the aorta. Complete occlusion would damage the walls of the aorta, red blood cells, and platelets.
When IABP is used, and when it’s not Indications
Cardiogenic Shock Pre-shock syndrome Threatening extension of MI Unstable angina Intractable ventricular dysrhythmias Septic Shock Cardiac Contusion Prophylactic support Bridging device to other mechanical assist Support during transport
When IABP is used, and when it’s not Contraindications
Absolute Aortic Valve insufficiency Dissecting aortic aneurysm Relative End-stage cardiomyopathies Severe atherosclerosis End stage terminal disease Abdominal aortic aneurysm Blood dyscrasias Thrombocytopenia
IABP As a Bridge to Cardiac Transplantation
15 to 30 % of end-stage cardiomyopathy patients awaiting transplantation need mechanical support
May decrease the need for more invasive LVAD support
The IABP has the following effects:
Increases coronary artery perfusion Increases myocardial oxygen supply Decreases myocardial oxygen demand Decreases myocardial work by reducing afterload Increases blood pressure Decreases Pulmonary artery pressure
Contraindications to IABP
Severe aortic insufficiency Aortic aneurysm Aortic dissection Limb ischemia Thromboembolism
IABP Kit Contents
Introducer needle Guide wire Vessel dilators Sheath IABP (34 or 40cc) Gas tubing 60-mL syringe Three-way stopcock Arterial pressure tubing (not in kit)
IAB Sizing Chart
The IAB Should be selected according to the following chart (chart located on every box).
Based on the height of the patient
Insertion Techniques
Percutaneous Sheath less Surgical insertion Femoral cut down Trans-thoracic
Positioning
The end of the balloon should be just distal to the takeoff of the left subclavian artery
Position should be confirmed by fluoroscopy or chest x-ray
Hemodynamics
Helium is rapidly pumped into and out of the balloon (about 40ccs). When inflated, this balloon displaces the blood that is in the aorta.
This is known as counter pulsation
Helium is used because it is a soluble gas and will not cause an embolus if the balloon ruptures
This sudden inflation moves blood superiorly and inferiorly to the balloon.
When the balloon is suddenly deflated, the pressure within the aorta drops quickly.
Hemodynamics (cont.)
Inflation of the balloon occurs at the onset of diastole. At that point, maximum aortic blood volume is available for displacement because the left ventricle has just finished contracting and is beginning to relax, the aortic valve is closed, and the blood has not had an opportunity to flow systemically.
The pressure wave that is created by inflation forces blood superiorly into the coronary arteries.
This helps perfuse the heart.
Blood is also forced inferiorly increasing perfusion to distal organs (brain, kidneys, tissues, etc.)
Hemodynamics (cont.)
The balloon remains inflated throughout diastole.
At the onset of systole, the balloon is rapidly deflated. The sudden loss of aortic pressure caused by the deflation reduces afterload.
The left ventricle does not have to generate as much pressure to achieve ejection since the blood has been forced from the aorta.
This lower ejection pressure reduces the amount of work the heart has to do resulting in lower myocardial oxygen demand.
IABP Summary Table
Aortic systolic pressure decreases Aortic diastolic pressure increases Cardiac output increases Cardiac afterload decreases Cardiac preload decreases
Timing
Inflation and deflation timing is critical in order to obtain the maximum benefits from the pump.
Incorrect timing can result in poor patient outcomes.
During a cardiac arrest, the IABP can provide very effective perfusion in conjunction with external compressions.
Since there is no ECG signal and no arterial pressure wave to trigger the pump, an internal trigger is selected.
This trigger detects the flow of blood caused by compressions and inflates the balloon providing improved circulation.
Good, consistent compressions are a must for this to work!
Use of the Autopulse in these situations has not been studied.
Triggering 5 ways triggering may be achieved
- ECG Uses R wave on the ECG to initiate the pumping.
- Pressure the arterial pressure waveform is used to trigger.
- Internal this allows a synchronous trigger set at 80 beats/min. Internal mode should never be used if a patient is generating a cardiac output.
- Pacer V/AV uses ventricular spike to trigger an event, is not an appropriate trigger for demand pacing.
- Pacer A the R wave on the ECG is the trigger, the atrial pacer spikes are enhanced and rejected.
This mode is only used if ECG trigger is not able to interpret R wave with A pacing. Never use if patient is ventricularly paced.
Inflation
Inflation is simply the expansion of the balloon catheter with helium, which is timed to just after the closure of the aortic valve. This is shown on the arterial waveform as the diacrotic notch. The diacrotic notch denotes closure of the aortic valve, when blood has been ejected from the (L) ventricle into the aorta. If inflated correctly a V shape should be shown on the balloon trace. The effect of displacement of blood in the aorta causes an increase in diastolic arterial pressure and an increase in cardiac output
Early Inflation
Inflation of the IAB prior to aortic valve closure.
Waveform Characteristics:
Inflation of IAB prior to dicrotic notch.
Diastolic augmentation encroaches onto systole, (may be unable to distinguish).
Physiologic effects:
Potential premature closure of the aortic valve.
Potential increase in LVEDV and LVEDP.
Increased left ventricular wall stress or afterload.
Aortic regurgitation.
Increased MV02 demand.
Worse to EARLY inflate than it is to LATE inflate
Late Inflation
Inflation of the IAB markedly after closure
of the aortic valve.
Waveform Characteristics:
Inflation of IAB after the dicrotic notch.
Absence of sharp V.
Physiologic Effects:
Sub-optimal coronary artery perfusion.
Deflation
Deflation is the depression of the balloon and the transfer of helium back into the console. Deflation of the IAB occurs in systole. Typically seen on the screen as being half way down the down slope after the diacrotic notch, prior to the aortic value opening. The effect is a decrease in aortic end diastolic pressure (afterload) by the balloon deflating and creating space in the aorta. This causes less impedence to blood being expelled from the left ventricle when the balloon is deflated. Results in an decreased ventricle wall tension, increased stroke volume and complete emptying of the ventricle. Cardiac work is reduced due to a decrease in left ventricular end systolic volume and preload, which reduces the cardiac work.
Early Deflation
Premature deflation of the IAB during the diastolic phase.
Waveform Characteristics:
Deflation of IAB is seen as a sharp drop following diastolic augmentation.
Sub-optimal diastolic augmentation.
Assisted aortic end diastolic pressure may be <= the unassisted aortic end diastolic pressure.
Assisted systolic pressure may rise.
Physiologic Effects:
• Sub-optimal coronary perfusion.
• Potential for retrograde coronary and carotid blood flow.
Sub-optimal after load reduction & Increased MV02 demand.
Late Deflation
Late deflation of the IAB during the diastolic phase.
Waveform Characteristics:
Assisted aortic end diastolic pressure may be equal to the unassisted aortic end diastolic pressure.
Rate of rise of assisted systole is prolonged.
Diastolic augmentation may appear widened.
Physiologic Effects:
Afterload reduction is essentially absent.
Increased MV02 consumption due to
the left ventricle ejecting against a
greater resistance
IAB may impede left ventricular ejection and increase the afterload
Complications
Limb ischemia Thrombosis Emboli Bleeding and insertion site Groin hematomas Aortic perforation and/or dissection Renal failure and bowel ischemia Neurologic complications including paraplegia Heparin induced thrombocytopenia Infection
Weaning of IABP
Timing of weaning Patient should be stable for 24-48 hours Decreasing inotropic support Decreasing pump ratio From 1:1 to 1:2 or 1:3 Decrease augmentation Monitor patient closely If patient becomes unstable, weaning should be immediately discontinued
Physician order MUST be obtained!
IAB Removal
Discontinue heparin six hours prior
Check platelets and coagulation factors
Deflate the balloon
Apply manual pressure above and below IABP insertion site
Remove and alternate pressure to expel any clots
Apply constant pressure to the insertion site for a minimum of 30 minutes
Check distal pulses frequently
ONLY pulled by cardiac NP/PA
Nursing Management of IABP
Hourly hemodynamics recorded
Hourly circulation observations
Hourly IABP ratio and level of augmentation
Nursed supine, 30o elevated or on side (ensuring that the leg which has the balloon inserted through the groin is straight at all times, avoid bending it.
Hourly urine output to indicate an early sign of IAB catheter migration.
Daily CXR to monitor position of IAB catheter
Observe insertion site for infection and bleeding.
Observe and maintain normal coagulation and electrolyte balance
Monitor and observe the external tubing from the catheter to pump for any condensation or bloodstains.
Ensure patient is quiet and relaxed with minimal movement around the bed. Sedation may be required.
Maintain a patient airway. The patient may be extubated if awake and orientated and satisfies extubation protocol.
