Upon completion of this course the student will be able to:
Define Preload and Afterload
List 2 Indications for Pulmonary Artery Catheter Insertion
List 2 Contraindications for Pulmonary Artery Catheter Insertion
Describe 3 Features of a Pulmonary Artery Catheter
State 2 Nursing Responsibilities During the Placement of a Pulmonary Artery Catheter
Have a better understanding of the steps required to float a Pulmonary Artery Catheter
List 3 Normal and Abnormal Hemodynamic Pressure Values
Give 2 reasons that might cause a damp Pulmonary Artery Waveform
Compare and contrast the effects of 2 different Vasopressors on Hemodynamic Pressure Values
The Factors that Determine Cardiac Output:
Cardiac output is the amount of blood (usually 4-8 liters per minute at rest) that is ejected from the heart. It is a product of stroke volume (the amount of blood ejected per beat) and heart rate. The following factors that play a significant role in a person’s stroke volume include:
Preload – This is the amount of stretch on the myocardial muscle fibers at the end of diastole. The volume of blood in the ventricles determines this stretch at any given time. Increased preload causes an increase in stroke volume, ventricular work and myocardial oxygen requirements while a decreased preload causes a decrease in stroke volume, ventricular work and myocardial oxygen requirement.
In the intensive care setting preload is measured by evaluating end-diastolic pressure measured by CVP (right atrial pressure for the right ventricle) and pulmonary artery pressure (PWP) which is the left ventricle. Preload can be manipulated to improve cardiac output and myocardial oxygenation with the use of fluid challenges, diuretics and vasodilators.
Afterload – This is the sum of all loads or forces against which the ventricular muscle fibers must shorten or push to eject blood into the arterial circulation. Increased or decreased afterload has the same effect on stroke volume, ventricular work and myocardial oxygen requirements as preload.
Left Ventricular Afterload is imposed mostly by aortic diastolic pressure and systemic vascular resistance
Right Ventricular Afterload is imposed mostly by pulmonary diastolic pressure and pulmonary vascular resistance
Contractility – This is the force and velocity of myocardial fiber shortening that is independent of preload and afterload. Positive inotropic stimuli with such medications as Epinephrine, Dopamine, and Digoxin increase the strength of contraction, myocardial work and myocardial oxygen consumption. The opposite occurs with the use of medications that have negative inotropic stimuli (beta blockers).
Note: Muscular synergy for efficient emptying requires muscle contraction to be smooth and unified. Cardiac disease, bundle branch blocks and ventricular arrhythmias can cause significant decreases in stroke volume.
Hemodynamic Monitoring:
The pulmonary artery catheter is a balloon-tipped multi-lumen catheter that allows for invasive hemodynamic monitoring. The primary purpose of invasive hemodynamic monitoring is the early detection, identification, and treatment of critically ill or injured patients. By using invasive hemodynamic monitoring the nurse is able to evaluate the patient's immediate response to treatment such as drugs and mechanical support.
Indications for Hemodynamic Monitoring:
Because there is no specific criteria or rule as to who should be hemodynamically monitored, each patient’s circumstance must be evaluated individually. The risk vs. benefit of placing a pulmonary artery catheter, as well as the expense need to be considered. General indications for pulmonary artery pressure monitoring include:
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)
Diagnostic indications (aspiration of arterial blood ,pulmonary hypertension)
Contraindications for placement of a pulmonary artery catheter include:
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
Pulmonary Artery Catheter Features (available for adults and pediatrics):
Length – 60 to 110 cm
Caliber – 4 to 8 French
Balloon inflation volume – 0.5 to 1.5 ml
Balloon diameter – 8 to 13 cm
Material – Polyvinyl Chloride
Catheter markings – black bands mark catheter in 10cm increments
Accessories – thermistor wire for measuring cardiac output, fiberoptics for measuring O2 and mixed venous saturation
Note: There are approximately 8 different types of pulmonary artery catheters, the most commonly used is the “Fiberoptic Thermodilution PAC” that has an additional lumen for medication administration and allows for continuous cardiac and mixed venous saturation monitoring.
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
Insertion Sites:
A pulmonary artery catheter (PAC) or Swan Ganz Catheter (SGC) is inserted into a major vein (subclavian, jugular or femoral) using an introducer sheath (this is the same sheath used to place a triple lumen catheter). Preference considerations for cannulation of the great veins are as follows:
Right Internal Jugular Vein (RIJ) – This is the shortest and straightest path to the heart
Left Subclavian vs. Right Subclavian- Compared to the right subclavian or left internal jugular vein, the left subclavian is an easier approach to the supra-vena cava as it is not necessary for the catheter to pass or course through any acute angles.
Femoral veins - These access points are distant sites, from which passing a SGC into the heart can be difficult, especially if the right-sided cardiac chambers are enlarged. Often, fluoroscopic assistance is necessary, but these sites are compressible and may be preferable if the risk of hemorrhage is high.
Preliminary Steps for Insertion and Floatation of PAC:
The bedside monitor and Continuous Cardiac Monitor should be turned on 10 to 15 minutes before insertion
Gather the following equipment:
Swan Ganz Catheter
Introducer Kit
Supplies to create a sterile field
Gowns, gloves and masks
Betadine (or other skin cleansing agent such as Chlorhexadrine)
4x4’s
Pressure bag
500ml NS or Heparin Premix
2 Disposable pressure monitoring kits with transducer (one for proximal and one for distal port)
Continuous cardiac output/Svo2 monitor with cables
IV solution for Cordis and medication line
Nursing Responsibilities Pre-Insertion:
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:
Position patient for insertion (flat for femoral, Trendenlenburg 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:
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:
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 Care of the Patient with a Pulmonary Artery Catheter:
Nursing care of the patient with a PAC can be very complex.Nursing management of these patients does not begin and end with writing numbers on a chart. The nurse must be able to interpret the data obtained as well as being able to alert medical staff of potential or actual complications. The following chart lists normal hemodynamic values.
Normal Hemodynamic Values
Hemodynamic Parameters
Abbreviations
Normal Values
Mean Arterial Pressure
MAP
70-90 mm Hg
Central Venous Pressure
CVP
2-8 mm Hg
Pulmonary Artery Systolic Pressure
PAS
20-30 mm Hg
Pulmonary Artery Diastolic Pressure
PAD
6-12 mm Hg
Pulmonary Artery Mean Pressure
MPAP
10-15 mm Hg
Pulmonary Artery Wedge Pressure
PAWP, Wedge
8-12 mm Hg
Cardiac Output
CO
4-8 L/min
Cardiac Index
CI
2.5-4 L/min
Stroke Volume
SV
60-130 ml
Stroke Volume Index
SVI
40-50 ml/m2
Systemic Vascular Resistance
SVR
800-1200 dynes
Systemic Vascular Resistance Index
SVRI
2000-2400 dynes
Pulmonary Vascular Resistance
PVR
150-300 dynes
Abnormal Hemodynamic Values:
Increased Systolic Pulmonary Artery Pressure can be 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 can be 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
Increased Pulmonary Artery Wedge Pressure (PAWP):
Left Heart Dysfunction
Mitral Stenosis/Regurgitation
Aortic Stenosis/Regurgitation
Decreased Left Ventricular Compliance
Intravascular Volume Overload
Tamponade/Effusion
Obstructive Left Atrial Myxoma
Restrictive Cardiomyopathy
Decreased Pulmonary Artery Wedge Pressure (PAWP):
Hypovolemia
Pulmonary Embolism
The Effects of Vasopressors on Hemodynamic Pressure Values:
Dopamine
Dopamine, a precursor of norepinephrine and epinephrine, is also a neurotransmitter. Dopamine is found in both the central and peripheral nervous systems and is released from nerve cells. Dopamine is indicated in the treatment of shock due to myocardial infarction, trauma, septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation. The effects of dopamine are complex and dose dependent. Dopamine directly stimulates dopaminergic receptors, alpha and beta adrenoceptors, and it indirectly causes the release of endogenous norepinephrine. At low doses (l to 5mcg/kg/minute), dopamine directly stimulates dopaminergic receptors on arteries in the kidneys, abdomen, heart, and brain and causes vasodilation. At these doses, urine output may increase, but blood pressure and heart rate are usually not affected. As the dose is increased (5 to 10 mcg/kg/min), dopamine stimulates beta 1 adrenoceptors, resulting in positive inotropic and chronotropic effects, which increases myocardial contractility, and heart rate, which results in, enhanced cardiac output. At higher doses (greater than 10 mcg/kg/min), dopamine exerts effects primarily alpha-receptors, and extensive vasoconstriction causes blood pressure to increase.
Levophed (Norepinephrine)
Norepinephrine is one of the principal neurotransmitters chemical substances involved in the transmission of nerve impulses in the sympathetic nervous system. It is released from nerve cells, and is indicated for the treatment of acute hypotension resulting from conditions such as spinal anesthesia, myocardial infarction, septicemia, blood transfusions, and drug reactions. This agent is also used adjunctively in the treatment of cardiac arrest and profound hypotension. Norepinephrine is a potent alpha adrenoceptor agonist and is therefore a strong vasoconstrictor, increasing systolic and diastolic blood pressures. In addition, Norepinephrine stimulates beta 1 cells so it increases both heart rate and contractility.
Dobutamine
Dobutamine is indicated for short-term inotropic support in patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgery. Classifying the drugs that have been discussed so far as vasopressors has been fairly straightforward. Including Dobutamine in this class of drugs is more difficult. Although Dobutamine is an inotrope, and considered by some to be avasopressor, others consider it a vasodilator. Dobutamine is generally considered a relatively selective beta adrenoceptor agonist because the net effect of Dobutamine administration is an increased cardiac contractility, decreased afterload and improved cardiac output.