Download File - Jessica Owen

Hemodynamic Monitoring
Jessica Owen
CCRN
Objectives
▪ Verbalizes purposes of Hemodynamic Monitoring
▪ Verbalize indications for Hemodynamic Monitoring
▪ Identify components of a Pulmonary Artery Catheter
▪ Identify the correct pressure waveforms
▪ Identify the components of invasive hemodynamic monitoring
▪ Identify “normal” parameters for each component of monitoring
▪ Verbalize how to troubleshoot abnormal waveforms
▪ Verbalize definition of preload and afterload
Definitions and Principles
• The measurement and interpretation of biological systems that describe
performance of the cardiovascular system
• Monitoring is NOT therapy
• Clinicians must know how to interpret the data
Purpose of Hemodynamic Monitoring
▪ Evaluate the cardiovascular system
▪ Establish baseline values and evaluate trends
– Single hemodynamic values are rarely significant. Look at trends!!
▪ Implement and guide interventions early to prevent problems
Hemodynamic Monitoring Components
▪ Heart Rate
▪ Blood Pressure and MAP
▪ CVP
▪ Pulmonary Artery Pressures
▪ Systemic Vascular Pressure (SVR)
▪ Pulmonary Vascular Pressure (PVR)
▪ Cardiac Output/ Cardiac Index
▪ Stroke Volume
Cardiac Output (L/min) = Heart Rate
(beats/min) x Stroke Volume (ml/beat)
Preload
Contractility
Afterload
Comparing Hemodynamics to an IV Pump
• Fluid = Preload
• Pump = Contractility (needs
electricity)
• Tubing = Afterload
Preload
•
Is the degree of muscle fiber stretching
present in the ventricles right before
systole
•
Is the amount of blood in a ventricle before
it contracts; also known as “filling
pressures”
•
Left ventricular preload is reflected by the
PCWP
•
Right ventricular preload is reflected by
the CVP
Cardiac Output reflects contractility if preload and afterload are optimized.
Cardiac Index is the cardiac output adjusted for body surface area (BSI).
Afterload
•
Any resistance against which the ventricles must
pump in order to eject its volume
•
How hard the heart [either side left or right] has
to push to get the blood out
•
Also thought of as the “ resistance to flow” or
how “clamped” the blood vessels are
•
SVR = Left ventricular afterload
•
PVR = Right ventricular afterload
Non-Invasive Hemodynamic Monitoring =
Clinical Assessment and NBP
Base Line Data
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General appearance
Level of consciousness
Skin color/temperature
Vital signs
Peripheral pulses
Urine output
Base line data should correspond with data obtained from technology
(i.e. ECG, ABP, CVP)
Limitations of Non- Invasive Blood Pressure
Limitations of NBP
▪ Cuff must be placed correctly and must be
appropriate size
▪ Auscultatory method is very inaccurate
– Korotkoff sounds difficult to hear
– Significant underestimation in low-flow (i.e.
shock) states
 Oscillometric measurements also commonly
inaccurate (> 5 mm Hg off directly recorded
pressures)
Indications for Arterial Blood Pressure
• Frequent titration of vasoactive drips
• Unstable blood pressures
• Frequent ABGs or labs
• Unable to obtain Non-invasive BP
Complications of Arterial Catheterization
•
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Hemorrhage
Hematoma
Thrombosis
Proximal or distal embolization
Pseudoaneurysm
Infection
Arterial Pressure Tracing
Waveform & Relationship to Cardiac Cycle
Waveform Distortion
Leveling and Zeroing
• Leveling
 Before/after insertion
 After patient, bed or transducer move
 Aligns transducer with catheter tip
• Zeroing
 Performed before insertion &
readings
• Level and zero transducer at the
phlebostatic axis
 4th intercostal space, mid-axillary line
 Level of the atria
Dynamic Flush
Dynamic flush ensures the
integrity of the pressure
tubing system.
Notice how it ascends –
forms a square pattern –
and bounces below the
baseline before returning
to the original waveform.
Check dynamic flush after
zeroing any pressure
system.
Central Venous Pressure
• CVP is a direct measurement of right ventricular end diastolic
•
•
•
•
•
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volume.
Assesses
 Intravascular volume status
 Right ventricular function
 Patients response to drugs &/or fluids
Central line or pulmonary artery catheter
Normal value = 2-8 mmHg
Low CVP = hypovolemia or ↓ venous return
High CVP = over hydration, ↑ venous return, or right-sided
heart failure
Always read CVP at end expiration
The Pulmonary Artery Catheter
PA Insertion Waves
PA Insertion Waves
Right Ventricular Waveform
• If the swan gets pulled
back into the RV it is
considered a swan
emergency.
• If you see an RV
waveform (looks like VT)
pull the swan
immediately.
• If the swan remains in
the RV it may cause the
patient to go into VT.
Complications of Pulmonary Artery Catheterization
• General central line complications
 Pneumothorax
 Arterial injury
 Infection
 Embolization
• Inability to place PAC into PA
• Arrhythmias (heart block)
• Pulmonary artery rupture
Components of PA Catheter (A.K.A. Swan-Ganz)
• Proximal port – (Blue) used to measure central venous pressure/RAP and
injection port for measurement of cardiac output
• Distal port – (Yellow) used to measure pulmonary artery pressure and
sample mixed venous blood
• Balloon port – (Red) used to determine pulmonary wedge pressure
• Thermistor lumen port near distal tip - monitors core temperature and
thermodilution method of measuring CO
Normal Hemodynamic Values
Mean Arterial Pressure (MAP)
60-100 mm Hg
Central Venous Pressure (CVP)
2-8 mm Hg
PAP Systolic (PAS)
20-30 mm Hg
PAP Diastolic (PAD)
5-15 mm Hg
PA Mean
15-25 mm Hg
Pulmonary Capillary Wedge Pressure (PWCP)
8-12 mm Hg
Cardiac Output
Cardiac Index
SVO2
4-8 L/min
2.5-4 L/min/M²
60-75%
Lactate Levels
< 2.0
Stroke Volume
50-100 ml
Systemic Vascular Resistance
900-1300
Cardiac Output Measurement
• Multiple techniques
 Thermodilution – most common
 Transpulmonary
• Pulse contour analysis
• Esophageal Doppler
• Newer pulmonary artery catheters offer continuous cardiac output
measurement
Thermodilution Method of Cardiac Output Measurement
CVP/PAWP
Volume Expanders:
Crystalloids & Colloids
Low
High
Preload
Vasopressors:
Alpha Stimulators
Positive Inotropics:
Beta-1 Stimulators
Phosphodiesterase
Inhibitors
Cardiac Glycosides
Positive Chronotropics:
Beta-1 Stimulators
Atropine
SVR/PVR
Afterload
Myocardial Contractility
Heart Rate
Diuretics
Venodilators
Arteriovasodilators:
Ca+ Channel Blockers
Alpha Inhibitors
Vascular Relaxants
Ace Inhibitors
Negative Inotopics:
Beta Blockers
Ca+ Channel Blockers
Negative Chronotropics:
Beta Blockers
Ca+ Channel Blockers
Vasopressors/Inotropes
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Dopamine
Dobutamine
Epinephrine
Phenylephrine
Norepinephrine
Vasopressin
Milrinone
Dopamine
(start at 1-5 mcg/kg/hr. max of 50)
adrenergic agonist agent
• Dose dependent receptor activation
 Low dose - increases blood flow via dopamine receptors in renal,
mesenteric, cerebral circulation
 Intermediate dose - increases cardiac output via ß- receptors
 High dose - progressive vasoconstriction via ą-receptors in systemic
and pulmonary circulation
• Tachyarrhythmias are most common complication (dose > 20 mcg/kg/hr)
• Low dose dopamine has no proven renal benefit
• Significant immunosuppressive effects through suppression of prolactin
from hypothalamus
Dobutamine
(2.5-20 mcg/kg/min max of 40)
adrenergic agonist agent
• Synthetic catecholamine generally considered the drug of choice for
severe systolic heart failure
• Increases cardiac output via ß1 -receptor and causes vasodilation via
ß2 -receptor
• Inotropic and chronotropic effects are highly variable in critically ill
patients
• Data supports use in septic shock when cardiac output remains low
despite volume resuscitation and vasopressor support
Epinephrine
(1-10 mcg/min or 0.1-0.5 mcg/kg/min)
alpha, beta agonist
• The most potent adrenergic agent available
• Potency and high risk of adverse effects limit use to cardiac arrest (and
specific situations after cardiac surgery)
• Primarily ß-receptor effects at low doses and ą-receptor effects at high
doses
• Drug of choice in anaphylactic shock
• Arrhythmogenic
Phenylephrine
(10-300 mcg/min)
adrenergic agonist
• Selective α1-adrenergic receptor agonist
• Little effect on the beta-receptors of the heart
• Contraindicated in severe arteriosclerotic cardiovascular and
cerebrovascular disease
• Complications include; arrhythmia (rare), decreased cardiac output,
hypertension, pallor, precordial pain or discomfort, reflex
bradycardia, severe peripheral and visceral vasoconstriction
Norepinephrine
(2-12 mcg/min max 30)
beta agonist
• More potent vasoconstrictor than dopamine; some inotropic effect
 Potent ą1 stimulation
 Moderate ß1 activity
 Minimal ß2 activity
• Use has changed from rescue drug in refractory septic shock to
primary agent
Vasopressin
(0.01-0.08 units/min)
• Antidiuretic hormone
• Acts on vascular smooth muscle via V1 receptors, independent of
adrenergic receptors
• Traditionally not titrated
• Significant splanchnic vasoconstriction
Milrinone
(0.125 – 0.75 mcg/kg/min)
phosphodiesterase 3 enzyme inhibitor
• Increases CI in patients with low CO
• Risk of ventricular arrhythmias including non-sustained VT
• Risk for excessive hypotension
Conclusion
• Multiple different methods of hemodynamic monitoring
• Keys to success
– Know when to use which method
– Technical skills for device placement
– Know how to interpret the data
• Remember the limitations of the technology