1. Functional Hemodynamic Indicators
Arterial Pressure Waveform Technology
Donna Adkisson, RN, MSN

2. Anatomy & Physiology Review
Blood Flow in the Heart
From the body
Right side of the Heart
To the lungs for Oxygenation
Air in via trachea
Bronchus
Bronchioles
Alveoli
Capillaries
Oxygen in
Carbon Dioxide out
Left side of the Heart
Out the aorta

3. Anatomy & Physiology Review
Cardiac Cycle
Diastole – relaxation or filling
Preload coming into right side of the heart
70% of blood flows into the ventricles passively
Other 30% from atrial kick
Systole – contraction or pumping
Atrial Systole = Ventricular Diastole
30% of blood flows into the ventricles from the atrial contraction
Ventricular Systole
How well can the heart pump – Ejection or Stroke Volume
What is the heart pumping against - SVR

4. Cardiac Output CO = SV x HR
Cardiac output is the volume of blood pumped by the heart per minute. For an average size of adult (70 kg) at rest this would be about 5 liters/min. During severe exercise it can increase to over 30 liters/min.
Cardiac output is frequently necessary to assess the state of a patient's circulation. The simplest measurements, such as heart rate and blood pressure, may be adequate for many patients, but if there is a cardiovascular abnormality then more detailed measurements are needed.

5. Hemodynamic Monitoring
Hemodynamic Monitoring is an important aspect of patient care in:
Operating Rooms
Critical Care Units
Hemodynamic Monitoring ranges from:
Non-Invasive Invasive
EKG NIBP Arterial Line LiDCO CVP PA catheter

6. Functional Hemodynamic Monitoring
Transpulmonary Thermodilution (TPTD)
– Based on the Stewart-Hamilton equation
LiDCOplus
Pulse Power analysis to derive Stroke Volume
Calibrated with Bolus dilution of lithium
PiCCO
Pulse contour analysis
Temperature change sensed by thermistor-tipped arterial catheter

7. Functional Hemodynamic Monitoring
Non-Calibrated
LiDCOrapid
Pulse Power analysis to derive Stroke Volume
Same algorithm as the LiDCOplus
FloTrac
Proprietary sensor attached to arterial line
Algorithm applied to analysis has been changed

8. Hemodynamic Monitoring including:
Cardiac Output
Cardiac Index
SVR
Stroke Volume
Blood Pressure
DO2
Oxygen Consumption
Preload Indicators

9. Cardiac Output Ways to clinically determine Cardiac Output:
Dilution method
Thermodilution
Green Dye
Lithium Dilution
Arterial Wave Form Analysis
Blood sample to calculate the Fick equation
Continuous Cardiac Output
TEE/EsopheagealDoppler

10. Continuous Cardiac Output?
Sampling to get a 3 to 5 minute average
PA catheter
Beat to Beat Continuous
Arterial wave form analysis

11. Beat-to-Beat Continuous Cardiac Output
Pulse Power waveform analysis continuously assesses the patient's hemodynamic status by analyzing and processing the arterial pressure signal obtained from the primary blood pressure monitor.

12. CO = SV x HR Stroke Volume Effected by:
The volume of blood per stroke of the heart
Effected by:
Amount of Blood coming into the heart – Preload
How well the heart works – Contractility
How much pressure or resistance the heart has to work against – Afterload

13. CO = SV x HR Stroke Volume SV = Preload + Afterload + Contractility
Preload – volume
Afterload – resistance (SVR)
Contractility – Muscle compliance (EF)

14. Ventricular Preload and Fluid Responsiveness
Fluid Resuscitation primary treatment of many shock states
Fluid Resuscitation is not without risk
Less than 50% of patients respond to a fluid bolus.
The heart performs more efficiently when appropriately filled.
The term preload refers to maximum stretch on the heart's muscle fibers at the end of diastolic filling. The degree of stretch is determined by the volume of blood contained in the ventricle at that time.

15. Ventricular Preload and Fluid Responsiveness
Commonly used static preload measurement are not sensitive or specific predictors of a patient's ability to respond to fluid bolus
CVP
PAOP
Functional Hemodynamic Indices are more sensitive and specific predictors of fluid responsiveness
Reflect the effect of positive pressure ventilation on preload and SV
Pulse Pressure Variation
Stroke Volume Variation
Systolic Pressure Variation

16. Functional Hemodynamics
Bridges, Elizabeth J. Arterial Pressure – Based Stroke Volume and Functional
Hemodynamic Monitoring. Journal of Cardiovascular Nursing,
March/April 2008;23(2): pp

17. Preload Systolic and Pulse pressure variation can be measured
intermittently from the arterial line via the beside monitor
continuously using
PPV, SVV or SPV
LiDCO system – plus or rapid
FloTrac
SVV

18. Preload Indicators
Systolic pressure variation (SPV) may reflect variations in pleural pressure and changing LVSV. PPV reflects only changes in transmural aortic pressure and therefore changes in LVSV on a beat-to-beat basis.  
Michard et al (1999) found PPV gave a more accurate measure of cardiac index when compared to SPV, which it turn was a better measure than CVP and PAW.
PPV was superior to SPV in predicting preload responsiveness proving to have better precision with less variance.
  Note: SPV and PPV do not require the patient to be in apnoea In fact they depend on positive pressure breathing.

19. Best Preload Responsiveness - PPV
Michard F., Boussat S, Chemla D, et al. Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure. American Journal of Respiratory and Critical Care Medicine. Jul 2000;162(1):

20. Hemodynamic Monitoring
Arterial Waveform Analysis
Preload indicator - looks at the variation from inspiration to expiration of the patient
PPV - Pulse Pressure Variation
Greater than 10 to 13% patient preload responsive
SVV - Stroke Volume Variation
Greater than 10 to 13% patient preload responsive
SPV - Systolic Pressure Variation
Greater than 5mmHg patient preload responsive

21. Frank Starling’s Law
The greater the ventricle is filled during diastole, the more the muscle fibres are stretched, the greater is the force of contraction.
This is true to a defined point of stretch above which point contraction force will not increase further.
The definition as put forward by Frank and Starling is :
The greater the ventricle is filled during diastole, the more the muscle fibres are stretched, the greater is the force of contraction. This is true to a defined point of stretch above which point contraction force will not increase further. So preload relates to the volume of blood filling the ventricle during diastole. A low preload will be caused by a low circulating volume and can decrease stroke volume and thus cardiac output

22. Frank Starling Curve Patient A is preload responsive
On steep part of curve
Set preload results in Significant increase in SV
Patient B is not preload responsive
An equal preloading does not result in a great increase in SV
This patient does not require fluid resuscitation
Patient B
 SV
 SV
 Preload
Patient A
Patient A is on the steep part of the curve representing a responder to fluid I.e giving fluid will increase stroke volume and thus cardiac output.
Increasing the BP is a secondary effect-we give fluid to increase the stroke volume.
Patient B is a non responder and giving the same amount of fluid will not increase the stroke volume greatly and may well not be of any benefit. The CVP nor PAWP tell us where we are on this curve but the stroke volume variation may well indicate where we are and thus guide fluid therapy.
 SV
 Preload

23. Case Studies Pulse Pressure Variation of 65%
After ½ liter of volume down to 24%
After another ½ liter of volume down to 10%
Pulse Pressure Variation of 124%
Patient on Epinephrine & Levophed drips
2 units of Albumin given
Within 24 hours, patient off all drips
Extubated
Pulse Pressure Variation of 38%, CO 2.8, EF 15%
Pulmonary Edema & Peripheral Edema
500cc IV fluid, Lasix (times 4)
8 hours later: PPV 16%, CO 3.9
no increase in Pulmonary or Peripheral Edema

24. Afterload Systemic Vascular Resistance
The amount of pressure the heart must work against
Decreases as CO & CI increases
Can be controlled with medications
Vasoconstrictor – Increases SVR & BP
Vasodialators – Decreases SVR & BP

25. Drugs used to Effect SVR
Vasoactive Drugs – can be a vasoconstrictor or vasodialators
Vasoconstrictors – increase SVR (afterload) and blood pressure, but vary in their effect on cardiac output. The pure a agonists leave the output of the normal heart unchanged, but may significantly reduce it in the failing heart. As the beta activity of the vasoconstrictor is increased, so cardiac output also tends to increase
Vasodilators – Used to dilate arteries, Decrease SVR, Decrease BP

26. Vasoactive Drugs Vasoactive Drugs: vasoconstructors
Isoproteranol – most widely used to ease breathing problems in asthma and COPD and to control irregular heartbeat until a pacemaker can be implanted.
Phenylephrine – Neo-Synephrine: used to treat shock and low blood pressure.
Ephedrine – used to counteract the hypotensive effects of anesthesia. Also useful as a pressor agent in hypotensive states following sympathectomy, or following overdosage drugs used for lowering blood pressure in the treatment of arterial hypertension.
Metaraminol – Aramine: used to raise the blood pressure and stimulate the heart in treating patients with shock.
Milrinone – Primacor : short-term treatment of patients with acute decompensated heart failure.
Vasopressin – an alternative to noradrenaline in the treatment of hypotension effective in combating milrinone-induced hypotension.

27. Drugs used to Effect SVR
Vasodilators - Used to dilate arteries, Decrease SVR, Decrease BP
Sodium Nitroprusside is the most potent of the 'mixed' vasodilators. Reliably reduces both afterload and preload.
Nitroglycerine acts predominantly on the venous side of the circulation to reduce preload. The reduction in preload is accompanied by a decrease in LV wall tension with a secondary reduction in myocardial oxygen, also a specific coronary arterial vasodilator and spasmolytic.
Adenosine can be used for its vasodilatory effects. Because of its short plasma half life (< 5 seconds), the drug has a particular role as a relatively specific pulmonary vasodilator.
Hydralazine acts exclusively on the arterial side of the circulation to reduce afterload.

28. Contractility Muscle Compliance (EF)
The ability of the muscle fiber to stretch and contract
Medications that can assist with contractility
Epinephrine
Dobutamine

29. Contractility Contractility Myocardial Contractility
Is the power of contraction
Is independent of preload or afterload
At a constant preload
positive inotropic agents > contractility > SV
Contractility
Contractility relates purely to the muscular power of the ventricular contraction and is independent of preload of afterload. A poorly functioning ventricle following ischaemic damage may have a loss of power-this relates to contractility.
bTo improve contractility inotropes are used. These increase the power of the contraction, increase the stroke volume but also increase the amount of oxygen the heart requires.

30. Drugs used to Effect Cardiac Output
Vasoactive Drugs – can be a vasoconstrictor or iontrope
Vasoconstrictors: increase SVR (afterload) and blood pressure, but vary in their effect on cardiac output. The pure a agonists leave the output of the normal heart unchanged, but may significantly reduce it in the failing heart. As the beta activity of the vasoconstrictor is increased, so cardiac output also tends to increase
Inotrope: is an agent that alters the force or energy of muscular contractions

31. Positive Inotropic Agents
Inotrope:
is an agent that alters the force or energy of muscular contractions
Adrenaline – Epinephrine (Epi or Adrenalin): used to treat shock, as a heart stimulant.
Noradrenaline – Norepinephrine (Levophed): used to increase the output of the heart and raise blood pressure as part of the treatment of shock.
Dopamine – used for the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarctions, trauma, endotoxic septicemia, open heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure.
Dobutamine – Dobutrex and generic forms: used to stimulate the heart during surgery or after a heart attack or cardiac arrest.

32. HR < 60 beats per minute HR > 100 beats per minute
CO = SV x HR
Heart Rate
HR < 60 beats per minute
HR > 100 beats per minute
Bradycardia – pacemaker, Atropine, Epinephrine
Tachycardia – Cardioversion, Digoxin, Treat fever or shock causing ↑ HR

33. Cardiac Output Changes
Cardiac Output Decreases
Decrease in blood volume
Increase in PPV or SVV
Decrease in ejection fraction
Decrease in SV
Decrease in Heart Rate
Bradycardia
Cardiac Output Increases
Vasodilation
Decrease in SVR
Increase in Contractility
Increase SV
Increase in Heart Rate
Tachycardiac

34. Decision Table www.lidco.com
Does my patient need an increase in SV or CO?
↓Yes
Is the arterial trace accurate?
Is the patient fully ventilated?
Is the tidal volume > 8ml/kg
Is the cardiac rhythm regular
What is the PPV or SVV
< 10% → No fluid > 10 to 13% → Give fluid

35. Fluid replacement therapy
Responder
Non responder
Stroke volume increases > 10%
Stroke volume increases < 10%
ml fluid challenge

36. The Old Way is Not Good Enough
Hemodynamic monitoring has traditionally involved the placement of a pulmonary artery catheter Minimally invasive Cardiac Output Monitoring eliminates the complications of the pulmonary artery catheter Which includes: Complications Related to Catheter Vascular Complications

37. Complications Related to Pulmonary Artery Catheters
Tachyarrhytmias
Right bundle branch block ( % )
Complete heart block ( with preexisting left bundle branch block )
Cardiac perfuration
Thrombosis and embolism
Pulmonary infarction due to persistent wedging ( 0-1.4% )
Catheter-related sepsis
PA rupture ( 0.2% chance )
Knotting of the catheter
Endocarditis, bland and infective
Pulmonic valve insufficiency
Balloon fragmentation and embolization

38. Vascular Complications Related to Pulmonary Artery Catheters
Accidental arterial puncture
Pneumothorax
Braquial plexus lesion
Horner syndrome
Phrenic nerve lesion
Gaseous embolism
Hemorrhage
Infections

39. Cost Related to Line Infections
Cost for Prolonged Bloodstream Infections can top $50,000 7 to 21 extra hospital days for Bloodstream Infections New Medicare Regulations Hospitals will no longer receive higher payments for the additional costs associated with treating patients for hospital-acquired infections Payments will be withheld from hospitals for care associated with treating vascular catheter-associated infections.
New rules go into effect October 2008

40. Cost Related to Line Infections
CDC reports that there are 248,678 cases of central line associated bloodstream infections every year. Institute for Healthcare Improvement estimates that approximately 14,000 people die every year from central line-related bloodstream infections.