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Hemodynamic Monitoring - 3 Nursing CEs 

Author: Kristi Hudson RN MSN CCRN

Written: January 9, 2005

Updated: September 11, 2009

 

Course Objectives

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)
  • Therapeutic indications (aspiration of  air emboli, cardiac pacing )
  • 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 a   vasopressor, 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.

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