1. Hemodynamic MonitoringBy
Nancy Jenkins RN,MSN

2. What is Hemodynamic Monitoring and why do it?
It is measuring the pressures in the heart
It allows us to see inside the heart and adjust volume as needed

3. Comparing Hemodynamics to IV pump
Fluid =preload
Pump= CO or contractility (needs electricity)
Tubing =afterload

4. Nursing Management Hemodynamic Monitoring- You are already doing
General appearance
Level of consciousness
Skin color/temperature
Vital signs
Peripheral pulses
Urine output
Lung sounds

5. Nursing Management Hemodynamic Monitoring
**Single hemodynamic values are rarely significant.
Monitor trends and evaluate whole clinical picture
Goals
Recognize early clues
Intervene before problems develop or escalate

6. Hemodynamic Monitoring Components We Will Look at Today
Heart Rate
Blood Pressure and MAP
CVP
Pulmonary Artery Pressures
Systemic Vascular Pressure (SVR)
Pulmonary Vascular Pressure (PVR)
Cardiac Output/ Cardiac Index
Stroke Volume

7. Important Equation

8. Hemodynamic Monitoring General Principles
CO: Volume of blood pumped by heart in 1 minute
CI: CO adjusted for body size
SV: Volume ejected with each heartbeat
SVI: SV adjusted for body size
Easier to adjust HR than SV
**Preload, afterload, and contractility determine SV

9. Hemodynamics: Normal value
Mean Arterial Pressure (MAP) mm Hg
Cardiac Index (CI) L/min/m2
Cardiac Output (CO)- 4-8 L/min
Central Venous Pressure (CVP) (also known as Right Atrial Pressure (RA)) 2-8 mmHg
Pulmonary Artery Pressure (PA)
Systolic mmHg (PAS) Diastolic 4-12 mmHg (PAD) Mean mmHg
Pulmonary Capillary Wedge Pressure (PWCP)
4-12 mmHg
Systemic Vascular Resistance(SVR)

10. Volume of blood within ventricle at end of diastole
**Measured by CVP and wedge pressure in ICU

11. Preload Def- the volume that stretches the LV just before contraction
Measured by CVP for RV and PAWP for LV
Measures the preload of the LV or LVEDP= wedge or PAW
**The greater the preload the greater the stroke volume and the greater the cardiac output

12. Decreased Preload- leads to Dec. SV and venous return
Hypovolemia
Tachycardia- why?
Vasodilation/ dec. venous return
Treatment- fluid
**A goal for heart failure

13. Increased Preload Valvular disease Hypervolemia Heart failure
Treatment- diuretics, vasodilators
**Vascular system holding tank- vasodilation, vasoconstriction depending on need

14. Measured by SVR and PVR in the ICU

16. Afterload Resistance to ejection- arterial B/P
Measured by PVR and SVR in the ER
Decreased afterload
Vasodilation (sepsis, hyperthermia)
Hypotention
Nitrates

17. Afterload Increased afterload
Vasoconstriction (hypovolemia, hypothermia)
Aortic stenosis
Hypertension
Fight or flight
Pulmonary hypertension
**The greater the afterload, the lower the cardiac output

18. Cardiac Output CO=SVxHR; CI= CO/BSA Normal CO 4-8 L/min; CI 2.2-4
Urine output- indirect measurement
To compensate for dec. CO get tachycardia
Decreased CO
Poor ventricular filling- hypovolemia or SVT
Poor emptying, dec. contractility (infarct, ischemia, arrhythmias)
Vasodilation- sepsis and drugs
Increased afterload- hypertension, vasoconstriction

19. Cardiac Output Increased Increased O2 demand- exercise SNS
Drugs- positive inotropics (Continuous infusions: Dobutamine, Dopamine, Primacor
Digoxin- IVP

20. Stroke Volume Def- amount of blood ejected with each heart beat
Normal SV=
Exercise can increase SV
Factors that determine SV
Preload
Afterload
Contractility

21. Contractility Starling’s law Increased contractility
SNS
Drugs- positive inotropics, epinephrine, calcium
Decreased contractility
Loss of muscle (acute MI, cardiomyopathy)
Hypoxemia
Electrolyte imbalance
Drugs- (lidocaine, calcium channel blockers, beta blockers

22. Contractility Determined by the SV and the EF%
**Important to know the EF% of all heart failure patients
Measured by echo
EF- how much blood is ejected during systole compared to how much preload there is.
**Normal EF% %
Ex 90/140= 64%EF

23. How and when do we measure afterload? Arterial B/P and SVR
Continuous arterial pressure monitoring
Acute hypertension/hypotension
Respiratory failure- frequent ABG sampling
Shock
Coronary interventional procedures
Continuous infusion of vasoactive drugs

24. Best indicator of tissue perfusion. Needs to be at
Best indicator of tissue perfusion. Needs to be at least to perfuse organs

26. Arterial Line

27. Arterial Pressure Monitoring
High- and low-pressure alarms based on patient’s status
Risks
Hemorrhage, infection, thrombus formation, neurovascular impairment, loss of limb
Nursing- Check 5 P’s

28. Arterial Pressure Waveform
Dicrotic notch signifies the closure of the aortic valve.

30. Pulmonary Artery Catheter
Fig. 66-7
PA Catheter Insertion

31. PPA catheter tells you everything you want to know about the heart: (Snap, Crackle, Pop)
-         1) how well the pump is pumping (cardiac output, cardiac index) (snap)
-          2)how full the right side of the heart is (CVP), and how full the left side is (wedge pressure) – that’s the volume…(crackle)
        3)  and how well your patient’s arteries can squeeze : that’s the SVR – the “systemic vascular resistance”… (pop)

35. PA Waveforms during Insertion
Fig. 66-9

38. Important Measurements Obtained by PA Catheter
Right Atrial Pressure (CVP)
PAP
Diastolic (PAD)
PA Systolic (PAS)
PA Wedge (Wedge, PAOP)
Cardiac Output
Cardiac Index

39. Pulmonary Artery Pressure Monitoring- CVP
Right atrium port- also know as proximal
Measurement of CVP
Injection of fluid for CO measurement
Can you give meds through this port?
Blood sampling

42. Central Venous Pressure Waveforms
Fig

43. CVP values Right Heart Presssures
Normal 2-8mmHg
Dec.
Hypovolemia
Decreased venous return
Inc.
Hypervolemia
Inc. venous return
Right HF, pulmonary hypertension
Tricuspid stenosis and regurgitation

44. PA pressure PAD- should be close to wedge PAS- tells RV pressure
PAW- LVEDP or preload of LV

47. PA Pressures Normal 20-30 mmHg systolic, 4-12mmHg diastolic
PAS= RV pressure
Inc PAS in pulmonary hypertension
Inc. PAD in ventricular failure
Dec. in hypovolemia
Dec. in shock

48. PAW Normal 6-12mmHg Equals LVEDP or preload of LV
Dec.in hypovolemia or low stroke volume
Inc. in LV failure, mitral valve disorders
Inc. in hypervolemia
*** Fluids for dec. wedge and diuretics for inc. wedge

50. Measuring Cardiac Output
Fig

51. Cardiac Output
Cardiac Output Monitoring

52. Measuring Cardiac Output and SVR
SVR can be calculated when CO is measured
SVR=(MAP-CVP) x80/ CO
↑ SVR
Vasoconstriction from shock
Hypertension
↑ Release or administration of epinephrine or other vasoactive inotropes
Left ventricular failure
Dec. SVR
Vasodilation
sepsis

53. Cardiac Output

55. Complications with PA Catheters
Infection and sepsis
Asepsis for insertion and maintenance of catheter and tubing mandatory
Change flush bag, pressure tubing, transducer, and stopcock every 96 hours
Air embolus (e.g., disconnection)

56. Complications with PA Catheters
Ventricular dysrhythmias
During PA catheter insertion or removal
If tip migrates back from PA to right ventricle
PA catheter cannot be wedged
May need repositioning

57. Complications with PA Catheters
Pulmonary infarction or PA rupture
Balloon rupture (e.g., overinflation)
Prolonged inflation
Spontaneous wedging
Thrombus/embolus formation

59. Noninvasive Hemodynamic Monitoring
Impedance cardiography (ICG)
Def-Continuous or intermittent, noninvasive method of obtaining CO and assessing thoracic fluid status
Impedance-based hemodynamic parameters (e.g., CO, SV, SVR) are calculated from Zo, dZ/dt, MAP, CVP, and ECG

60. Noninvasive Hemodynamic Monitoring
Major indications
Early signs and symptoms of pulmonary or cardiac dysfunction
Differentiation of cardiac or pulmonary cause of shortness of breath
Evaluation of etiology and management of hypotension

61. Noninvasive Hemodynamic Monitoring
Major indications (cont’d)
Monitoring after discontinuing a PA catheter or justification for insertion of a PA catheter
Evaluation of pharmacotherapy
Diagnosis of rejection following cardiac transplantation

62. hemodynamic cases (1 and 4)
Case Study

63. Three main types of hypotension (“shock states”) that you’re going to see in the ICU
1. “Pump”- Cardiogenic shock
2. “Volume”- Hypovolemia
3. Squeeze” - Sepsis

64. - Pump” problems. “Cardiogenic” shock
-         Pump” problems? “Cardiogenic” shock? The cardiac output will be low, because the pump isn’t pumping. Blood pressure drops. The body says to itself: “What to do? Got to keep the blood pressure up somehow!”, and starts to tighten up the arterial bed. What number tells how tight the arterial system is? – SVR.
So – in cardiogenic shock, the cardiac output goes down, the SVR goes up – the pattern is usually plain as day. “Ooh, look! The output is only 2.2, and the SVR is 2400!” What does the wedge pressure do? (Remember, the LV is pumping poorly, and can’t empty itself…)

65. - “Volume” problems. “Hypovolemic” shock. Lost a lot of blood
-         “Volume” problems? “Hypovolemic” shock? Lost a lot of blood? Running too many marathons? Cardiac output will probably be low, since there isn’t enough volume to pump with. CVP and wedge pressures? Low, right? – again, not enough volume. SVR? Same as cardiogenic: the arteries clamp down, trying to maintain pressure.
Hypovolemic shock: cardiac output low, central pressures low, SVR high.

66. Septic shock: cardiac output high, central pressures low, SVR low.
-         “Squeeze” problem? Any idea what makes this happen? Anybody say, “sepsis”? All that bacteremic endotoxin makes the arteries dilate – blood pressure drops. What to do? Now the body uses the mirror reflex of what it did in the cardiogenic setting: instead of clamping down the arteries, which it can’t do, because that’s where the problem is – now the heart picks up the slack, pumping both faster and harder: heart rate goes up, and cardiac output does too.
Septic shock: cardiac output high, central pressures low, SVR low.