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Flashcards in Week 7 Hemodynamics Deck (146):
1

Hemodynamics is

The study of the motion of blood through the body.

2

Fundamental Concepts of hemodynamics

Cardiac Output
Preload
Afterload
Contractility

3

Normal Hemodynamic Values SVO2

60-75%

4

Normal Hemodynamic Values Stroke Volume

50-100ML

5

Normal Hemodynamic Values Stroke Index

25-45mL/M2

6

Normal Hemodynamic Values Cardiac Output

4-8 L/min

7

Normal Hemodynamic Values MAP

60-100mm Hg

8

Normal Hemodynamic Values CVP

1-7mm Hg

9

Normal Hemodynamic Values PAP systolic

20-30mm Hg

10

Normal Hemodynamic Values PAP Diastolic

5-15 mm Hg

11

Normal Hemodynamic Values PAOP (wedge)

8-12 mm Hg

12

Normal Hemodynamic Values SVR

900-1300 dynes.sec.com

13

Cardiac Output

The cardiac output pushes the blood through the vascular system.
Cardiac output (CO) is calculated by multiplying the heart rate (HR) by the stroke volume (SV).
Stroke volume is the volume of blood pumped out of the heart with each heartbeat.
If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output.
This is known as compensatory tachycardia.
heart rates greater than 150 bpm actually drop stroke volume

14

Cardiac Index =

CO/BSA=2.4 - 4.0L/min/m2

BSA = height in c weight in k divide by 360 then divide all that by 2

15

Stroke volume is affected by three factors:

preload, afterload, and contractility

16

Compensatory tachycardia

If the stroke volume drops, the body will compensate by increasing the heart rate to maintain cardiac output.

17

Preload

the amount of stretch on the cardiac myofibril at the end of diastole.
When the ventricle is at its fullest

18

Preload is most directly related to:

Fluid volume

19

Starling's curve:

describes the relationship of preload to cardiac output
As preload (fluid volume) increases, cardiac output will also increase until the cardiac output levels off.
If additional fluid is added after this point, cardiac output begins to fall.

20

Preload Measurement

Not measured directly...instead measured by physical assessment of fluid volume

21

Signs of inadequate preload include:

Poor skin turgor
Dry mucous membranes
Low urine output
Tachycardia
Thirst
Weak pulses
Flat neck

22

Signs of excess preload in a patient with:

distended neck veins
crackles in the lungs
Bounding pulses

23

Increased preload in a patient with poor cardiac function presents with

crackles in the lungs
S3 heart sound,
low urine output
Tachycardia
cold clammy skin with weak pulses
edema

24

Preload

Insufficient preload is commonly called hypovolemia or dehydration.
Insufficient volume is present in the vascular tree, the sympathetic nervous system is stimulated to release the atecholamines, epinephrine and norepinephrine.
These hormones cause increased heart rate and arterial vasoconstriction.
The increased heart rate produces a compensatory tachycardia while the vasoconstriction helps maintain an adequate blood pressure.
If these patients are treated with catecholamine drugs rather than receiving volume infusions, the tachycardia becomes very pronounced and the vasoconstriction can become severe enough that the organs fail and the distal extremities become ischemic.

25

The first step in treating any form of hemodynamic instability is:

to assess the patient for signs of insufficient preload (e g volume or blood loss)

26

Afterload is:

the resistance that the ventricle must overcome to eject its volume of blood.

27

The most important determinant of afterload is

vascular resistance

28

Other factors affecting afterload include:

blood viscosity
aortic compliance
valvular disease.

29

As arterial vessels constrict, what happens to afterload?

the afterload increases

30

As arterial vessels dilate, what happens to afterload?

the afterload decreases

31

Increased CO

higher volumes

32

Decreased CO

decreased volumes

33

In general, when you have someone with signs of low preload treat with

volume, until you know if its a stretch issue

34

High Afterload:

increases myocardial work and decreases stroke volume.

35

Patients with high afterload present with signs and symptoms of arterial vasoconstriction including

cool clammy skin
capillary refill greater than 5 seconds
narrow pulse pressure.

36

Pulse pressure is calculated by:

subtracting the diastolic blood pressure (DBP) from the systolic blood pressure (SBP).

37

What is normal pulse pressure at the brachial artery

40 mm Hg

38

Low afterload:

myocardial work and results in increased stroke volume.

39

Patients with low afterload present with symptoms of arterial dilation

warm flushed skin
Bounding pulses
wide pulse pressure

40

If the afterload is too low, what may result?

hypotension

41

Points to ponder for afterload:

A key component of treatment for heart failure is afterload reduction using beta-blockers and ACE inhibitors.
By decreasing the resistance to ventricular ejection the cardiac output is increased and myocardial workload is decreased.
The increase in cardiac output frequently improves the functional status of these patients.

ACE inhibitors
Beta blockers

42

Contractility refers to

the inherent ability of the cardiac muscle to contract regardless of preload or afterload status.

43

Contractility is enhanced by

exercise, catecholamines, and positive inotropic drugs.

44

Contractility is decreased by

by hypothermia, hypoxemia, acidosis, and negative inotropic drugs.

45

Myocardial compliance refers to

the ventricle’s ability to stretch to receive a given volume of blood.

Normally the ventricle is very compliant so large changes in volume will produce small changes in pressure.
If compliance is low, small changes in volume will result in large changes in pressure within the ventricle.
If the ventricle cannot stretch, it will be unable to increase cardiac output with increased preload.

46

Tissue perfusion is the

transfer of oxygen and nutrients from the blood to the tissues.

47

When performing interventions designed to improve hemodynamics

valuation of effectivess is whether or not the intervention was successful in improving tissue perfusion.

48

Many of the signs of inadequate preload, afterload and contractility also reflect poor tissue perfusion.

Cool clammy skin
Cyanosis
Low urine output
Decreased level of consciousness
Metabolic acidosis
Tachycardia
Tachypnea
Hypoxemia

49

Labs and diagnostic testing that are used to evaluate tissue perfusion include

Arterial blood gases
Arterial lactate levels
Pulse oximetry.
Poor tissue perfusion is reflected by a low pH, low base excess and elevated lactate level.
Pulse oximetry readings are typically low when tissue perfusion is compromised to a significant degree.

50

Methods of Hemodynamic Monitoring

Arterial Blood Pressure
Central Venous Pressure/ Right Atrial Pressure
The Pulmonary Artery Catheter
Cardiac Output Measurement
Tissue Oxygenation

51

Arterial Blood Pressure

Non-invasive
MAP most accurate
Direct arterial pressure measurement

52

Reasons for Hemodynamic Monitoring

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 (cardiac pacing )
Diagnostic indications (pulmonary hypertension)

53

Arterial Blood Pressure Site Selection; The most preferred insertion site

is the radial artery

54

alternate Arterial blood pressure sites include

the femoral and brachial arteries.
The femoral artery is not a preferred site due to its anatomic location.

55

if the radial artery is used

Assess site with modified Allen test
performed prior to cannulation to ensure that the ulnar artery provides adequate circulation to the hand to prevent tissue ischemia or necrosis.

56

Indications for Arterial Catheterization Need for continuous blood pressure measurement

Hemodynamic instability
Vasopressor requirement

MAP should be 60-100mm/Hg

57

Indications for arterial catheterization Respiratory failure

Frequent arterial blood gas assessments

58

Indications for Arterial Catheterization most common locations

radial, femoral, axillary, and dorsalis pedis

59

What size is the art line catheter

The intra-arterial catheter is typically a 20-gauge intravenous-type catheter

60

What is important about the art line transducer?

must be level with the art line insertion site!!! If not you will get false readings

61

Obtaining Blood Draws from the A-Line

Using proper technique when obtaining blood from an intra-arterial catheter:
Maintain aseptic technique for any line access and use standard precautions

Withdraw blood gently and slowly from the line

Waste the first 5mL

Flush the collection port to prevent clot formation and bacterial colonization

Maintain sterility of the system; place a new sterile cap over the sample port

Fast-flush the system to the patient for no more than 3 seconds at a time

Do not use a syringe to manually flush arterial catheters

Manual flushing with a syringe generates enough pressure that the injected fluid can invade the cerebral circulation

62

Complications of Arterial Catheterization

Hemorrhage
Hematoma
Thrombosis
Proximal or distal embolization
Pseudoaneurysm
Infection

63

Limitations of Arterial Catheterization

Pressure does not accurately reflect flow when vascular impedance is abnormal
Systolic pressure amplification
Mean pressure is more accurate

Recording artifacts
Underdamping
Overdamping

64

Central Venous Catheterization:Central venous pressure

Right atrial (superior vena cava) pressure

Limited by respiratory variation and PEEP

65

Central Venous Catheterization: Central venous oxygen saturation

SCVO2

Correlates with SMVO2 assuming stable cardiac function

66

Central Venous Pressure Waveform: The central venous catheter

may be a large or small-bore catheter with one or more lumens inserted via the subclavian, internal jugular or external jugular vein.

67

Right Atrial Pressure Monitoring Indications

Measure right atrial pressure (RAP)
Same as Central Venous Pressure (CVP)
1-7 mm Hg

Assess blood volume; reflects preload to the right side of the heart

Assess right ventricular function

Infusion site for large fluid volume

Infusion site for hypertonic solutions

68

Reasons for elevated CVP/ RA pressure:

decreased right (or single) ventricle compliance
tricuspid valve disease
Intravascular volume overload
cardiac tamponade
tachyarrhythmia

69

Reasons for reduced RA pressure:

low intravascular volume status

inadequate preload

70

Right Atrial Pressure Monitoring Waveform Analysis
a wave:

rise in pressure due to atrial contraction

71

Right Atrial Pressure Monitoring Waveform Analysis
c wave

rise in pressure due to ventricular contraction and closure of the tricuspid valve

72

Right Atrial Pressure Monitoring Waveform Analysis
x decent

fall in pressure due to atrial relaxation increase in atrial pressure

73

Right Atrial Pressure Monitoring Waveform Analysis
v wave

rise in pressure during atrial filling
passive filling

74

Right Atrial Pressure Monitoring Waveform Analysis
y decent

all in pressure due to opening of the tricuspid valve and onset of ventricular filling(passive)

75

Right Atrial Pressure Monitoring Waveform Analysis
Elevated RAP

RV failure
Tricuspid regurgitation
Tricuspid stenosis
Pulmonary hypertension
Hypervolemia
Cardiac tamponade
Chronic LV failure
Ventricular Septal Defect
Constrictive pericarditis

76

Right Atrial Pressure Monitoring Waveform Analysis
Decreased RAP

Hypovolemia
Increased contractility

77

The Pulmonary Artery Catheter

Widespread use in critically ill patients
Remains controversial

78

The Pulmonary Artery Catheter measures

CVP
PAP
PAOP
Cardiac Index
SVO2

79

How many PACs are inserted annually?

approximately 1 million

80

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

81

Nursing Responsibilities Pre-Insertion PAC

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)

82

Nursing Responsibilities During Insertion PAC

Position patient for insertion (flat for femoral, Trendelenburg 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

83

Nursing Responsibilities Post-Insertion PAC

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

84

Nursing Documentation Post-Insertion PAC

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

85

Nursing Responsibilities For Removal

Make sure the balloon is COMPLETELY deflated. Pull back extra, then lock.

When removing, if piece of catheter is left in patient, IMMEDIATELY put patient in trendelenburg and place pt on left side.

86

Increased Systolic Pulmonary Artery Pressure 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

87

Increased Diastolic Pulmonary Artery Pressure 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

88

Pulmonary Artery Systolic and Diastolic Pressure Decreased

Hypovolemia

Severe Tricuspid or Pulmonic Stenosis

89

Changes in PAWP Increased

Left Heart Dysfunction
Mitral Stenosis/Regurgitation
Aortic Stenosis/Regurgitation
Decreased Left Ventricular Compliance
Intravascular Volume Overload
Tamponade/Effusion
Obstructive Left Atrial Myxoma
Restrictive Cardiomyopathy

90

Changes in PAWP Decreases

Hypovolemia
Pulmonary Embolism

91

Complications of Pulmonary Artery Catheterization: General central line complications

Pneumothorax
Arterial injury
Infection
Embolization

92

Other Complications of Pulmonary Artery Catheterization:

Inability to place PAC into PA
Arrhythmias (heart block)
Pulmonary artery rupture

93

Contraindications...when would you not want to place a PAC

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

94

Thermodilution Method of Cardiac Output Measurement

Measuring Cardiac Output
Inject fluid in to r atrium, fluid migrates through, change in temp over time and tells you how well the heart is contracting

95

Tissue Oxygenation

Despite advances, our ability to monitor the microcirculation and tissue perfusion is limited
Laboratory tests for metabolic acidosis are global and insensitive
Newer technology
Gastric tonometry reads the co2 in the stomach, helps determine acidotic state
Sublingual capnometry

96

Nursing HOURLY assessment:

Air in line or stopcocks
Precipitates
Leaking at site
Increasing resistance
Condition of entrance sites

97

Equipment Used in Hemodynamic Monitoring:Semi-rigid pressure tubing

attaches the catheter to a transducer set-up.
The tubing must be more rigid than standard IV tubing so that the pressure of the fluid within it does not distort the tubing.
If the tubing is distorted in this way, the pressure readings will be inaccurate.
The tubing must also be as short as reasonably possible.
Longer tubing will cause distortion of the pressure as it travels over the longer distance.

98

Equipment Used in Hemodynamic Monitoring: transducer

a device that converts the pressure waves generated by vascular blood flow into electrical signals that can be displayed on electronic monitoring equipment.

99

Equipment Used in Hemodynamic Monitoring: transducer cable

attaches the transducer to the monitor, which displays a pressure waveform and numeric readout.

100

Equipment Used in Hemodynamic Monitoring: flush system

consists of a pressurized bag of normal saline (which may or may not contain added heparin, depending on the unit and facility where you work).
The pressure must be maintained at 300 mm Hg to prevent blood from the arterial system from backing up into the pressure tubing.

101

Equipment Used in Hemodynamic Monitoring: intraflow valve

part of the transducer setup and maintains a continuous flow of flush solution (approximately 3-5 ml/hr) into the monitoring system to prevent clotting at the catheter tip.

102

Equipment Used in Hemodynamic Monitoring: fast flush device

allows for general flushing of the system and rapid flushing following withdrawal of blood from the system or when performing a square wave test.

103

Transducer Leveling: phlebostatic axis

located at the 4th intercostal space, halfway between the anterior and posterior chest (mid-chest).

104

Derived Pressures

Cardiac Index (CI)

Stroke Volume (SV) – CO/HR

Stroke Volume Index (SVI) – CI/HR

MAP- SBP + 2(DBP)/3

Systemic Vascular Resistance (SVR)- (MAP-RAP) x 80/CO

Systemic Vascular Resistance Index (SVRI) - (MAP-RAP) X80/CI

105

Hemodynamic Emergencies: LV Failure

HR ↑
MAP
CO
CVP/RAP
PAP/PAWP
Notes

106

Hemodynamic Emergencies: Pulmonary Embolism

HR ↑
MAP
CO
CVP/RAP
PAP/PAWP
Notes

107

Hemodynamic Emergencies: Cardiogenic pulmonary edema

HR ↑
MAP
CO
CVP/RAP
PAP/PAWP
Notes

108

Hemodynamic Emergencies: cardiac tamponade

HR ↑
MAP
CO
CVP/RAP
PAP/PAWP
Notes

109

Hemodynamic Emergencies : RV Failure

HR ↑ or varies
MAP
CO
CVP/RAP
PAP/PAWP
Notes

110

Hemodynamic Emergencies : Cardiogenic Shock

HR ↑
MAP
CO
CVP/RAP
PAP/PAWP
Notes

111

Hemodynamic Emergencies : Septic Shock

HR ↑
MAP
CO
CVP/RAP
PAP/PAWP
Notes

112

Hemodynamic Emergencies: Hypovolemic Shock

HR ↑
MAP
CO
CVP/RAP
PAP/PAWP
Notes

113

Vasopressors/Inotropes

Dopamine
Dobutamine
Epinephrine
Phenylephrine
Norepinephrine
Vasopressin

114

Dopamine

Dose dependent receptor activation

Low dose (1-5mics) - increases blood flow via dopamine receptors in renal, mesenteric, cerebral circulation

Intermediate dose (5-10mics) - increases cardiac output via - receptors

High dose(>10mics) - progressive vasoconstriction via -receptors in systemic and pulmonary circulation

In vivo, receptor effects are often mixed
Tachyarrhythmias are most common complication
Low dose dopamine has no proven renal benefit
Significant immunosuppressive effects through suppression of prolactin from hypothalamus

115

Dobutamine

Synthetic catecholamine generally considered the drug of choice for severe systolic heart failure

Increases cardiac output via Beta 1 -receptor and causes vasodilation via Beta 2 -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

116

Epinephrine

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 Beta receptor effects at low doses and alpha receptor effects at high doses
Arrhythmogenic

117

Phenylephrine

Relatively pure beta adrenergic agonist
Minimal inotropic effects; often causes reflex bradycardia
Consistently decreases cardiac output
Increased propensity to cause ischemic complications
Be wary in the OR

118

Norepinephrine

More potent vasoconstrictor than dopamine; some inotropic effect
Potent alpha 1 stimulation
Moderate beta 1 activity
Minimal beta 2 activity

119

Vasopressin

Acts on vascular smooth muscle via V1 receptors, independent of adrenergic receptors
Considered replacement therapy
Traditionally not titrated
Significant splanchnic vasoconstriction

120

Intra-Aortic Balloon Pump (IABP)

The Intra-Aortic Balloon Pump (IABP) is a circulatory assist device that is used to support the left ventricle.

121

Principles of the IABP

A flexibile catheter is inserted into the femoral artery and passed into the descending aorta.
Correct positioning is critical in order to avoid blocking off the subclavian, carotid, or renal arteries.
When inflated, the balloon blocks 85-90% of the aorta. Complete occlusion would damage the walls of the aorta, red blood cells, and platelets.

122

When IABP is used, and when it’s not Indications

Cardiogenic Shock
Pre-shock syndrome
Threatening extension of MI
Unstable angina
Intractable ventricular dysrhythmias
Septic Shock
Cardiac Contusion
Prophylactic support
Bridging device to other mechanical assist
Support during transport

123

When IABP is used, and when it’s not Contraindications

Absolute
Aortic Valve insufficiency
Dissecting aortic aneurysm
Relative
End-stage cardiomyopathies
Severe atherosclerosis
End stage terminal disease
Abdominal aortic aneurysm
Blood dyscrasias
Thrombocytopenia

124

IABP As a Bridge to Cardiac Transplantation

15 to 30 % of end-stage cardiomyopathy patients awaiting transplantation need mechanical support
May decrease the need for more invasive LVAD support

125

The IABP has the following effects:

Increases coronary artery perfusion
Increases myocardial oxygen supply
Decreases myocardial oxygen demand
Decreases myocardial work by reducing afterload
Increases blood pressure
Decreases Pulmonary artery pressure

126

Contraindications to IABP

Severe aortic insufficiency
Aortic aneurysm
Aortic dissection
Limb ischemia
Thromboembolism

127

IABP Kit Contents

Introducer needle
Guide wire
Vessel dilators
Sheath
IABP (34 or 40cc)
Gas tubing
60-mL syringe
Three-way stopcock
Arterial pressure tubing (not in kit)

128

IAB Sizing Chart

The IAB Should be selected according to the following chart (chart located on every box).

***Based on the height of the patient***

129

Insertion Techniques

Percutaneous
Sheath less
Surgical insertion
Femoral cut down
Trans-thoracic

130

Positioning

The end of the balloon should be just distal to the takeoff of the left subclavian artery
Position should be confirmed by fluoroscopy or chest x-ray

131

Hemodynamics

Helium is rapidly pumped into and out of the balloon (about 40ccs). When inflated, this balloon displaces the blood that is in the aorta.
This is known as counter pulsation
Helium is used because it is a soluble gas and will not cause an embolus if the balloon ruptures
This sudden inflation moves blood superiorly and inferiorly to the balloon.
When the balloon is suddenly deflated, the pressure within the aorta drops quickly.

132

Hemodynamics (cont.)

Inflation of the balloon occurs at the onset of diastole. At that point, maximum aortic blood volume is available for displacement because the left ventricle has just finished contracting and is beginning to relax, the aortic valve is closed, and the blood has not had an opportunity to flow systemically.
The pressure wave that is created by inflation forces blood superiorly into the coronary arteries.
This helps perfuse the heart.
Blood is also forced inferiorly increasing perfusion to distal organs (brain, kidneys, tissues, etc.)

133

Hemodynamics (cont.)

The balloon remains inflated throughout diastole.
At the onset of systole, the balloon is rapidly deflated. The sudden loss of aortic pressure caused by the deflation reduces afterload.
The left ventricle does not have to generate as much pressure to achieve ejection since the blood has been forced from the aorta.
This lower ejection pressure reduces the amount of work the heart has to do resulting in lower myocardial oxygen demand.

134

IABP Summary Table

Aortic systolic pressure decreases
Aortic diastolic pressure increases
Cardiac output increases
Cardiac afterload decreases
Cardiac preload decreases

135

Timing

Inflation and deflation timing is critical in order to obtain the maximum benefits from the pump.
Incorrect timing can result in poor patient outcomes.
During a cardiac arrest, the IABP can provide very effective perfusion in conjunction with external compressions.
Since there is no ECG signal and no arterial pressure wave to trigger the pump, an internal trigger is selected.
This trigger detects the flow of blood caused by compressions and inflates the balloon providing improved circulation.
Good, consistent compressions are a must for this to work!
Use of the Autopulse in these situations has not been studied.

136

Triggering 5 ways triggering may be achieved

1. ECG Uses R wave on the ECG to initiate the pumping.

2. Pressure the arterial pressure waveform is used to trigger.

3. Internal this allows a synchronous trigger set at 80 beats/min. Internal mode should never be used if a patient is generating a cardiac output.

4. Pacer V/AV uses ventricular spike to trigger an event, is not an appropriate trigger for demand pacing.

5. Pacer A the R wave on the ECG is the trigger, the atrial pacer spikes are enhanced and rejected.
This mode is only used if ECG trigger is not able to interpret R wave with A pacing. Never use if patient is ventricularly paced.

137

Inflation

Inflation is simply the expansion of the balloon catheter with helium, which is timed to just after the closure of the aortic valve. This is shown on the arterial waveform as the diacrotic notch. The diacrotic notch denotes closure of the aortic valve, when blood has been ejected from the (L) ventricle into the aorta. If inflated correctly a V shape should be shown on the balloon trace. The effect of displacement of blood in the aorta causes an increase in diastolic arterial pressure and an increase in cardiac output

138

Early Inflation

Inflation of the IAB prior to aortic valve closure.

Waveform Characteristics:
Inflation of IAB prior to dicrotic notch.
Diastolic augmentation encroaches onto systole, (may be unable to distinguish).

Physiologic effects:
Potential premature closure of the aortic valve.
Potential increase in LVEDV and LVEDP.
Increased left ventricular wall stress or afterload.
Aortic regurgitation.
Increased MV02 demand.

Worse to EARLY inflate than it is to LATE inflate

139

Late Inflation

Inflation of the IAB markedly after closure
of the aortic valve.
Waveform Characteristics:
Inflation of IAB after the dicrotic notch.
Absence of sharp V.
Physiologic Effects:
Sub-optimal coronary artery perfusion.

140

Deflation

Deflation is the depression of the balloon and the transfer of helium back into the console. Deflation of the IAB occurs in systole. Typically seen on the screen as being half way down the down slope after the diacrotic notch, prior to the aortic value opening. The effect is a decrease in aortic end diastolic pressure (afterload) by the balloon deflating and creating space in the aorta. This causes less impedence to blood being expelled from the left ventricle when the balloon is deflated. Results in an decreased ventricle wall tension, increased stroke volume and complete emptying of the ventricle. Cardiac work is reduced due to a decrease in left ventricular end systolic volume and preload, which reduces the cardiac work.

141

Early Deflation

Premature deflation of the IAB during the diastolic phase.

Waveform Characteristics:

Deflation of IAB is seen as a sharp drop following diastolic augmentation.
Sub-optimal diastolic augmentation.
Assisted aortic end diastolic pressure may be <= the unassisted aortic end diastolic pressure.
Assisted systolic pressure may rise.

Physiologic Effects:
• Sub-optimal coronary perfusion.
• Potential for retrograde coronary and carotid blood flow.
Sub-optimal after load reduction & Increased MV02 demand.

142

Late Deflation

Late deflation of the IAB during the diastolic phase.
Waveform Characteristics:
Assisted aortic end diastolic pressure may be equal to the unassisted aortic end diastolic pressure.
Rate of rise of assisted systole is prolonged.
Diastolic augmentation may appear widened.
Physiologic Effects:
Afterload reduction is essentially absent.
Increased MV02 consumption due to
the left ventricle ejecting against a
greater resistance
IAB may impede left ventricular ejection and increase the afterload

143

Complications

Limb ischemia
Thrombosis
Emboli
Bleeding and insertion site
Groin hematomas
Aortic perforation and/or dissection
Renal failure and bowel ischemia
Neurologic complications including paraplegia
Heparin induced thrombocytopenia
Infection

144

Weaning of IABP

Timing of weaning
Patient should be stable for 24-48 hours
Decreasing inotropic support
Decreasing pump ratio
From 1:1 to 1:2 or 1:3
Decrease augmentation
Monitor patient closely
If patient becomes unstable, weaning should be immediately discontinued

Physician order MUST be obtained!

145

IAB Removal

Discontinue heparin six hours prior
Check platelets and coagulation factors
Deflate the balloon
Apply manual pressure above and below IABP insertion site
Remove and alternate pressure to expel any clots
Apply constant pressure to the insertion site for a minimum of 30 minutes
Check distal pulses frequently

ONLY pulled by cardiac NP/PA

146

Nursing Management of IABP

Hourly hemodynamics recorded

Hourly circulation observations

Hourly IABP ratio and level of augmentation

Nursed supine, 30o elevated or on side (ensuring that the leg which has the balloon inserted through the groin is straight at all times, avoid bending it.

Hourly urine output to indicate an early sign of IAB catheter migration.

Daily CXR to monitor position of IAB catheter

Observe insertion site for infection and bleeding.

Observe and maintain normal coagulation and electrolyte balance

Monitor and observe the external tubing from the catheter to pump for any condensation or bloodstains.

Ensure patient is quiet and relaxed with minimal movement around the bed. Sedation may be required.

Maintain a patient airway. The patient may be extubated if awake and orientated and satisfies extubation protocol.