1. Pulmonary Artery Catheters: Putting the Numbers and the Waveforms Together
John Whitlock, MS, RN
Nurse Specialist Cardiac Surgery
Barbara Regan, BSN, RN
Unit Based Educator Cardiac Surgery

2. Disclosures
No Disclosures
No Conflicts of Interest

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JOHNW421

4. Objectives Review of basic hemodynamics
Normal waveforms
Normal values
Examine changes in hemodynamics and waveforms in the context of:
Anatomical changes
Disease states
Provide 3 case studies for discussion

5. Hemodynamic Basics Waveforms make sense!
Fluid pressures change with mechanical activity
When a heart chamber contracts, the pressure goes up
When a chamber relaxes, the pressure goes down
When a valve closes the pressure goes down
Abnormalities of the heart or valves will change the appearance of the waveform
Clinical conditions will increase or decrease the values

6. Pulmonary Artery Catheters

7. The Waveforms
This Photo by Unknown Author is licensed under CC BY-SA-NC

8. Normal Pressures

9. Normal Values
SVO % Stroke volume mL Stroke index mL/M2 Cardiac output 4-8 L/min Cardiac index L/min/M2 Mean Arterial Pressure (MAP) mm Hg Central Venous Pressure (CVP or RAP) 2-6 mm Hg Pulmonary Artery Systolic (PAS) mm Hg Pulmonary Artery Diastolic (PAD) 5-15 mm Hg PAWP (Wedge) 8-12 mm Hg Systemic Vascular Resistance (SVR) dynes.sec.cm5 Pulmonary Vascular Resistance (PVR) dynes.sec.cm5

10. Central Venous Pressure

11. Absent a Wave
Atrial Fibrillation

12. Prominent a Wave
Tricuspid Stenosis

13. Cannon a Wave
Junctional Rhythm

14. Tricuspid Regurgitation
Regurgitant c Wave
Tricuspid Regurgitation

15. Conditions effecting the CVP waveform
Absent a wave
Atrial fibrillation
Prominent a wave
Tricuspid stenosis
Cannon a wave
Tricuspid regurgitation
Junctional rhythm
Regurgitant c wave

16. Abnormal CVP Waveforms
CONDITION
CHARACTERISTICS
Atrial Fibrillation
Loss of “a” wave
Prominent “c” wave
AV Dissociation
Cannon “a” wave
Tricuspid Regurgitation
Tall systolic “c-v” wave
Loss of “x” descent
Tricuspid Stenosis
Tall “a’ wave
Attenuation of “y” descent
RV Ischemia
Tall “a” and “v’ waves
Steep “x’ and “y” descents
Pericardiac Constriction
Tall “a” and “v” waves
Steep “x” and “y” descents
Cardiac Tamponade
Dominant “x” descent
Attenuated “y” descent

17. Pulmonary Artery Pressure

18. Arterial Waveform

19. Pulmonary Artery Wedge Pressure

20. Pulmonary Artery Diastolic
PAD and PCWP have a very close and reliable relationship.
If PAD rises, we can assume that PCWP has gone up

21. Pulmonary Hypertension
Increased pressure in the pulmonary vasculature results in:
Higher PA systolic AND diastolic. May have wider pulse pressure if primary pulmonary
Larger waveform due to higher pressure
Resembles arterial waveform
Higher CVP because of the backup of blood as RV starts to fail
a, c, and v waves may be less distinct
May or may not see increased ABP
Fibrotic disease does not effect systemic pressure until late stages
ESLD will result in portal hypertension which leads to pHTN
PCWP will seem very low compared to PA because of normal LV

22. Cardiac Tamponade
Constricted heart can not contract and relax normally
ABP falls due to low output
Pulse pressure narrows
CVP rises due to blood backing up
a, c, and v waves are pronounced at first, then dampen
PA pressures begin to equalize with systemic pressures as the tamponade progresses
Waveform becomes less distinct as external pressures rise
PCWP
Rises with increased external pressure

23. Heart Failure HFpEF versus HFrEF HFrEF
HFrEF will present with more changes and subtle changes mean more!
HFrEF
ABP will be low
Combination of low output and intentional decreased afterload
Narrow pulse pressure
CVP often elevated
Small changes can be significant
Waveform often dampened
PA may or may not be elevated
LV and RV roles
Waveform variable
PCWP sensitive indicator of LV function
Rises with worsening function

24. Case Study
Your patient is a 42 year-old female 3 Days postop from Mitral valve replacement. Her Swan-Ganz catheter was left in because her CVP remained elevated despite diuresis.
Her vital signs are:
37.6°C
HR 68 Sinus rhythm
119/64 MAP 82
RR 18 unlabored SaO2 100%
CVP 8
PAP 53/24 mPA 34
PCWP 10

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28. Case Study PMH PSH Breast CA 10 years ago 35 pack year smoker HTN
Currently not smoking
HTN
Managed with ACE inhibitor
PSH
Lumpectomy left breast
Hernia repair

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31. Case Study
Your patient is an 84 year old male admitted for urosepsis. He had a Pulmonary Artery Catheter placed this morning because his MAP continued to worsen despite starting Phenylephrine and adding Norepinephrine.
His vitals signs are:
38°C
HR 110 Sinus tachycardia
96/54 MAP 68 on low dose Phenylephrine and Norepinephrine
RR 20 unlabored SaO2 on 2L NC
CVP 8
PAP 28/12 mPA 16
PCWP 8

32. Case Study
PMH
STEMI with DES placed in LAD and circumflex arteries
GERD
Type I diabetes A1c 7.5
60 units of Lantus at night and Novolog with meals
PSH
Hiatal hernia repair 10 years ago
THR 4 years ago
Teeth extracted last year

33. Case Study
You notice that his CVP waveform has changed slightly on the monitor. This is what you see:

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36. Case Study
Your patient is a 56 year old man admitted for acute decompensated heart failure (HFrEF). He has had a Pulmonary Artery Catheter since yesterday morning and, with aggressive diuresis, his CVP has dropped from 16 to 10 and his SvO2 has improved from 55% to 67%.
His vitals signs are:
37°C
AV paced at 80
100/50 MAP 67
RR 20 unlabored SaO2 on 4L NC
CVP 10
PAP 30/15 mPA 16
PCWP 12

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39. References
Torres, A. J. (2018). Hemodynamic assessment of atrial septal defects. Journal of Thoracic Disease, 10, S2882–S Perel, A., Saugel, B., Teboul, J.-L., Malbrain, M., Belda, F., Fernández-Mondéjar, E., … Fernández-Mondéjar, E. (2016). The effects of advanced monitoring on hemodynamic management in critically ill patients: a pre and post questionnaire study. Journal of Clinical Monitoring & Computing, 30(5), 511– Saugel, B., Flick, M., Bendjelid, K., Critchley, L. A. H., Vistisen, S. T., & Scheeren, T. W. L. (2019). Journal of clinical monitoring and computing end of year summary 2018: hemodynamic monitoring and management. Journal of Clinical Monitoring & Computing, 33(2), 211– AACN, & Wiegand, D. (2017). AACN Procedure Manual for High Acuity, Progressive and Critical Care. St. Louis, MO: Elsevier/Saunders. Yartsef, A. ( ) Deranged Physiology: A Free Online Resource for Intensive Care Medicine. Retrieved on May 15, 2019 from