Cardiogenic shock an IABP

1. CARDIOGENIC SHOCK
AND IABP
PRESENTER: Ms. PRIYANKA BHATI MODERATOR:
Ms. SMITA DAS
M.Sc. Nursing 2nd year Lecturer, CON,
AIIMS

2. CS is caused by severe impairment of myocardial performance
that results in diminished cardiac output, end-organ
hypoperfusion, and hypoxia.
Clinically this presents as hypotension refractory to volume
resuscitation with features of end-organ hypoperfusion
requiring pharmacological or mechanical intervention.
Acute myocardial infarction (MI) accounts for 81% of patient in
CS.
INTRODUCTION

3. DEFINATION
The clinical
definition of
cardiogenic
shock is
Decreased
cardiac
output and
Evidence of
tissue
hypoxia
In the
presence of
adequate
intravascular
volume.
Hemodynamic criteria for cardiogenic shock are
sustained hypotension (systolic blood pressure < 90 mm
Hg for ≥30 min)
And a reduced cardiac index (< 2.2 L/min/m2)
in the presence of normal or elevated pulmonary
capillary wedge pressure (>15 mm Hg) or Right
ventricular end-diastolic pressure (RVEDP) (>10 mm Hg).

5. EPIDEMIOLOGY
Complication of Acute MI.(5-10%) Is the leading cause of death after
MI.
Higher incidences of CS in women, Asian/Pacific Islanders .
patients aged >75 years.
ST-segment–elevation myocardial infarction (STEMI) is associated
with a 2-fold increased risk for development of CS compared with
non– ST-segment–elevation myocardial infarction (NSTEMI).
While the in-hospital mortality has improved, the 6- to 12-month
mortality in cardiogenic shock has remained unchanged at 50% over
the past 2 decades.
Survivors of MI-associated CS have an 18.6% risk of 30-day
readmission after discharge, with a median time of 10 days.

6. RISK FACTORS
If Patient have a heart attack, risk of developing cardiogenic shock
increases.
Older age .
History of heart failure or heart attack.
blockages (coronary artery disease) in heart's main arteries.
diabetes or high blood pressure.
As female sex.

7. CAUSES OF CARDIOGENIC SHOCK
The causes of cardiogenic shock are known as either coronary or non-coronary.
Coronary. Coronary cardiogenic shock is more common than noncoronary cardiogenic
shock and is seen most often in patients with acute myocardial infarction.
Noncoronary. Noncoronary cardiogenic shock is related to conditions that stress the
myocardium as well as conditions that result in an ineffective myocardial function.
C.S can result from any condition that causes significant left ventricular dysfunction
with reduced cardiac output.
Myocardial infarction (MI).Regardless of the underlying cause, left ventricular
dysfunction sets in motion a series of compensatory mechanisms that attempt to
increase cardiac output, but later on leads to deterioration.
Myocardial ischemia. Compensatory mechanisms may initially stabilize the patient but
later on would cause deterioration with the rising demands of oxygen of the already
compromised myocardium.
End-stage cardiomyopathy.The inability of the heart to pump enough blood for the

8. PATHOPHYSIOLOGY

9. PHYSICAL EXAMINATION CLINICAL
FINDINGS
Patients in shock usually appear ashen or cyanotic and have cool
skin and mottled extremities.
Peripheral pulses are rapid and faint and may be irregular if
arrhythmias are present.
Jugular venous distention and crackles in the lungs are usually
(but not always) present; peripheral edema also may be present.
Heart sounds are usually distant, and third and fourth heart
sounds may be present.
Pulse pressure may be low, and patients are usually tachycardic.
Patients show signs of hypoperfusion, such as altered mental
status and decreased urine output.

10. Systolic murmur is generally heard in patients with acute mitral
regurgitation or ventricular septal rupture.
SIGNS AND SYMPTOMS
The diagnosis of cardiogenic shock can sometimes be made at
the bedside by observing the following:
Hypotension.
Absence of hypovolemia.
Clinical signs of poor tissue perfusion (ie, oliguria, cyanosis,
cool extremities, altered mentation).

11. DIAGNOSIS AND INVESTIGATION

12. DIAGNOSTIC CONSIDERATIONS
Conditions to consider in the differential diagnosis of cardiogenic shock
include the following:
Systemic inflammatory response syndrome (SIRS)
Acute coronary syndrome (ACS)
Aortic regurgitation
Dilated cardiomyopathy
Restrictive cardiomyopathy
Congestive heart failure (CHF) and pulmonary edema
Mitral regurgitation
Pericarditis and cardiac tamponade
Hypovolemic shock
Papillary muscle rupture
Acute valvular dysfunction

13. LABORATORY FINDINGS
White blood cell count and C-reactive protein typically are
elevated.
Renal function often is progressively impaired.
Hepatic transaminases are elevated due to liver hypoperfusion
in ~20% of patients and may be very high.
The arterial lactate level is usually elevated to >2 mmol/L.
ABGs usually demonstrate hypoxemia and anion gap metabolic
acidosis.
Glucose levels at admission are often elevated, a strong
independent predictor for mortality.
Cardiac markers, creatine kinase and its MB fraction, and

14. ELECTROCARDIOGRAM
In acute MI with CS, Q waves and/or ST elevation in multiple
leads or left bundle branch block are usually present.
Approximately one-half of MIs with CS are anterior infarctions.
Global ischemia due to severe left main stenosis usually is
accompanied by aVR lead ST segment elevation and ST
depressions in multiple leads.

15. CHEST ROENTGENOGRAM
The chest x-ray typically shows pulmonary vascular
congestion and often pulmonary edema, but may be normal in
up to a third of patients.
The heart size is usually normal when CS results from a first
MI, but may be enlarged when it occurs in a patient with a
previous MI.

16. ECHOCARDIOGRAM
An echocardiogram should be obtained
promptly in patients with
suspected/confirmed CS to help define its
etiology.
Echocardiography is able to delineate the
extent of infarction/myocardium in jeopardy
and the presence of mechanical complications
such as VSR, MR, or cardiac tamponade.
Valvular obstruction or insufficiency, dynamic
LV outflow tract obstruction, proximal aortic
dissection with aortic regurgitation or
tamponade may be seen, or indirect evidence
for pulmonary embolism may be obtained .

17. Clinical Question Information
Ventricular Function Predominantly left, right or biventricular involvement
Etiology Acute Myocardial Infarction
•Extent of infarction/myocardium in jeopardy
•Status of the non-culprit infarct zone
•Presence of mechanical complications
Acute/ChronicValvular Insufficiency/Obstruction/Stenosis (Native/Prosthetic)
•Etiology: endocarditis; degenerative valve disease
•Location and hemodynamic consequences
Dynamic LeftVentricularTract Obstruction
Takotsubo Syndrome
CardiacTamponade
•Circumferential versus localized effusion
•Route of pericardiocentesis if indicated
Acute Pulmonary Embolism
•Right ventricular function
•Pulmonary artery pressure
•Presence of clot in transition/Patent foramen ovale
Acute Aortic Syndrome
•Nature and extent of dissection
•Degree of aortic insufficiency
•Presence of pericardial effusion

18. Hemodynamics Volume assessment by inferior vena cava diameter and
inspiratory collapse
Estimated pulmonary artery systolic pressure
Estimated left atrial pressure
Therapeutic
guidance
Guide vasoactive support
Monitor response to therapy
Mechanical circulatory support decisions
Catheter position and guidance
Pulmonary Pleural effusion
Lung edema
Pneumothorax
Pulmonary infiltration

19. OTHER IMAGING STUDIES
Ultrasonography can be used to guide fluid
management.
Coronary angiography is urgently indicated in patients
with myocardial ischemia or MI who also develop
cardiogenic shock.

20. PULMONARY ARTERY
CATHETERIZATION
PAC hemodynamic monitoring is declining because clinical trials have
shown no mortality benefit.
Hemodynamic data provided by a PAC can confirm the presence and
severity of CS, involvement of the right ventricle, left-to-right
shunting, pulmonary artery pressures and trans-pulmonary gradient,
and the pulmonary and systemic vascular resistance.
It can help in recognition of acute MR, decreased left atrial filling
pressure, and secondary occult sepsis and to exclude left-to-right
shunts.
The detailed hemodynamic profile can be used to individualize and
monitor therapy and to provide prognostic information, such as cardiac
index and cardiac power, can be obtained.

22. DIAGNOSIS AND MANAGEMENT
IN EMERGENCY
For unstable patients
supportive therapy must be initiated simultaneously with
diagnostic evaluation .
A focused history and physical examination should be
performed along with an electrocardiogram (ECG), chest X-ray,
arterial blood gas (ABG) analysis, lactate measurement, and
blood specimens to the laboratory.
Initial echocardiography is an invaluable tool to elucidate the
underlying cause of CS.

23. EMERGENCY MANAGEMENT

24. TREATMENT- MEDICAL
MANAGEMENT
It is an emergency necessitating immediate resuscitative therapy before
shock irreversibly damages vital organs.
The aim of treatment is to enhance cardiovascular status by:
Oxygen. Oxygen is prescribed to minimize damage to muscles and
organs.
Pain control. In a patient that experiences chest pain, IV morphine is
administered for pain relief.
Hemodynamic monitoring. An arterial line is inserted to enable accurate
and continuous monitoring of BP and provides a port from which to
obtain frequent arterial blood samples.
Fluid therapy. Administration of fluids must be monitored closely to
detect signs of fluid overload.

25. CONSIDERATIONS FOR INITIAL
CRITICAL CARE MONITORING IN
PATIENTS WITH CS

29. INITIAL VASOACTIVE MANAGEMENT
CONSIDERATIONS IN TYPES OF CS

32. DIURETICS
Mainstay of therapy to treat pulmonary edema and augment urine
output
No good data regarding optimal diuretic protocol or whether diuretics
improve outcome in renal failure
Lower doses of lasix are needed to maintain urine output when
continuous infusions are used
Start at 5 mg/hr, can increase up to 20 mg/hr

33. CRITICAL CARE COMPLICATION PREVENTION BUNDLES IN PATIENTS
WITH CS

34. MECHANICAL VENTILATION
The reported prevalence of MV is 78% to 88% in patients with
CS, and it is often required for the management of
 Acute hypoxemia,
 Increased work of breathing,
 Airway protection, and
 Hemodynamic or electric instability.

35. REPERFUSION-
REVASCULARIZATION
Rapid revascularization of the infarct-related artery is the only
evidence-based treatment strategy for mortality reduction in CS and
forms the mainstay therapeutic intervention for CS due to MI.
In the SHOCK Trial 132 lives were saved per 1000 patients treated with
early revascularization with percutaneous coronary intervention (PCI) or
coronary artery bypass graft (CABG) compared with initial medical
therapy.
In general, PCI with drug-eluting stents of the infarct-related artery is
the preferred reperfusion strategy.
 Approximately 80% of CS patients present with multivessel coronary
artery disease.

36. CONT…
The recent CULPRIT-SHOCK randomized trial showed that
culprit lesion only PCI with possible staged revascularization led
to a reduction in 30-day mortality or renal replacement therapy
in comparison to immediate multivessel PCI.
This reduction in the primary study endpoint was mainly
driven by a 30-day mortality reduction.
Currently, vascular access for diagnostic angiography and PIC
via the radial artery is preferred when feasible over femoral
arterial access due to its greater safety.

37. CORONARY ARTERY BYPASS
Critical left main artery disease and three-vessel coronary
artery disease (CAD) are common findings in patients who
develop cardiogenic shock.
The potential contribution of ischemia in the non infarcted
zone contributes to the deterioration of already compromised
myocardial function.
CABG in the setting of cardiogenic shock is generally
associated with high surgical morbidity and mortality rates.
CABG is currently performed in only 5% of cases mainly if
coronary anatomy is not amenable to PCI.

38. MECHANICAL CIRCULATORY
SUPPORT AND CARDIAC
TRANSPLANTION
The most commonly used mechanical circulatory support (MCS) device
has been the intra aortic balloon pump (IABP), which is inserted into the
aorta via the femoral artery and provides passive hemodynamic support.
IABP also had no benefit on secondary endpoints (arterial lactate,
catecholamine doses, renal function, or intensive care severity of illness
unit scores).
IABP is no longer recommended for CS with LV failure.
Active MCS devices to support the left, right, or both ventricles can be
placed percutaneously or surgically.
Temporary percutaneous MCS can be used as bridge to recovery, to
surgically implanted devices, to heart transplantation, or as a
temporizing measure when the neurologic status is uncertain.

39. THE USE OF THE IABP REDUCES SYSTOLIC LV AFTERLOAD AND
AUGMENTS DIASTOLIC CORONARY PERFUSION PRESSURE, THEREBY
INCREASING CARDIAC OUTPUT AND IMPROVING CORONARY ARTERY
BLOOD FLOW.

40. CONT…
Percutaneous MCS including the Tandem Heart, Impella
devices, and also venoarterial extracorporeal membrane
oxygenation (VA-ECMO) have been used in patients not
responding to standard treatment (catecholamines, fluids, and
IABP) and also as a first-line treatment.
Active percutaneous MCS results in better hemodynamic
support compared to IABP.
Surgically implanted devices can support the circulation as
bridging therapy for cardiac transplant candidates or as
destination therapy.

41. CONTINUOUS RENAL
REPLACEMENT THERAPY
Among patients with CS, a reported 13% to 28% develop acute
kidney injury and up to 20% require renal replacement therapy.
Patients needing renal replacement therapy were less likely to
survive to hospital discharge and had a higher risk of long-term
dialysis and mortality.
Patients with CS often do not hemodynamically tolerate fluid
shifts that can occur with intermittent haemodialysis.
Instead, continuous renal replacement therapy, which applies a
veno-venous driving force with an external pump to gradually
removal fluid and toxins, is more commonly used for those with
CS.

42. COMMON OPTIONS FOR
NONDURABLE PERCUTANEOUS
MCS.

43. LEFT VENTRICULAR ASSIST DEVICES
Standard
Percutaneous
 Tandem Heart
 Complete support
 Trans septal puncture
 Need good RV function
 Impella
 Complete support
 Easy to insert
 Also need good RV function

44. TANDEM HEART™
 Continuous flow
 Removes oxygenated blood
from LA via trans-septal
catheter placed through
femoral vein
 Returns blood via femoral
artery
 Shown to
 ↓ LAP and PCWP
 ↓ MVO2
 ↑ MAP, CO

45. IMPELLA
 Continuous flow
 Inserted into LV
through AV
 Blood returns to
descending aorta
 Not yet approved in
US

46. DURABLE MCS
Long-term MCS as a Bridge to transplantation (BTT) was first approved by
the US Food and Drug Administration in 1998.
All currently used durable MCS devices are continuous-flow devices,
include an inflow cannula placed directly into the LV cavity and an outflow
graft sutured into the ascending aorta, and can provide hemodynamic
support with flow rates ranging from 5 to 10 L/min.
The HeartMate II (St. Jude Medical) is approved for BTT and destination
therapy and uses an axial-flow pump, whereas the Heart Ware HVAD
(HeartWare, Framingham, MA), which is approved as a BTT device, uses only
a centrifugal-flow, hydrodynamically levitated pump.

48. RV SUPPORT
MCS options for the temporary management of RV failure
(including RV infarction) are currently being developed and
studied.
The Impella RP (Abiomed Europe) is an intracardiac micro-axial
blood pump that can be inserted percutaneously though the
femoral vein.
When properly positioned, this catheter can deliver blood from
the inlet area (in the inferior vena cava), through the cannula,
and into the pulmonary artery with an intent to restore right-
sided heart hemodynamics, to reduce RV workload, and to allow
cardiac recovery.

49. HEART TRANSPLANTATION
Cardiac transplantation, particularly for patients requiring
biventricular MCS, often represents the only hope for meaningful,
long-term recovery.
Unfortunately, the low number of available organs, coupled with
unpredictable donor availability, makes heart transplantation in the
acute setting of CS an unreliable primary therapy.

50. NOVEL THERAPIES AND
OPPORTUNITIES
Therapeutic hypothermia for post-MI cardiogenic shock has multiple
potentially beneficial physiologic effects, including the potential to
improve post-ischemic cardiac function and hemodynamics, decrease
myocardial damage, and reduce end-organ injury from prolonged
hypoperfusion.
The newly introduced HeartMate Percutaneous Heart Pump features a
novel design with a collapsible elastomeric impeller and nitinol
cannula, which gives this device a low profile but high flow rate

52. PALLIATIVE CARE IN CS
Palliative care can reduce physical and emotional distress, improve
quality of life, and complement curative therapy in advanced HF.

54. NURSING MANAGEMENT
Nursing Assessment
The nurse should assess the following:
Vital signs: Assess the patient’s vital signs, especially the blood
pressure.
Baseline and subsequent findings and individual hemodnamic
parameters, heart and breath sounds, ECG pattern,
presence/strength of peripheral pulses, skin/tissue status, renal
output, and mentation.
Respiratory rate, character of breath sounds, frequency, amount,
and appearance of secretions, presence of cyanosis, laboratory
findings, and mentation level.
Fluid overload: The ventricles of the heart cannot fully eject the
volume of blood at systole, so fluid may accumulate in the lungs.

55. NURSING DIAGNOSIS
Based on the assessment data, the major nursing diagnoses are:
1. Decreased cardiac output related to changes in myocardial
contractility/inotropic changes
2. Impaired gas exchange related to changes in alveolar-capillary membrane.
3. Excess fluid volume related to a decrease in renal organ perfusion,
increased sodium and water, hydrostatic pressure increase, or
decrease plasma protein.
4. Ineffective tissue perfusion related to reduction/cessation of blood flow.
5. Acute pain related to ischemic tissues secondary to blockage or narrowing
of coronary arteries.
6. Activity intolerance related to imbalance between the oxygen supply and

56. NURSING CARE PLANNING &
GOALS
The major goals for the patient are:
Prevent recurrence of cardiogenic shock.
Monitor hemodynamic status.
Administer medications and intravenous fluids.
Maintain intra-aortic balloon counterpulsation.

57. NURSING INTERVENTION
Intra-aortic balloon counter-pulsation: The nurse makes ongoing timing
adjustments of the balloon pump to maximize its effectiveness by
synchronizing it with the cardiac cycle.
Enhance safety and comfort: Administering of medication to relieve
chest pain, preventing infection at the multiple arterial and venous
line insertion sites, protecting the skin, and monitoring respiratory and
renal functions help in safeguarding and enhancing the comfort of the
patient.
Arterial blood gas: Monitor ABG values to measure oxygenation and
detect acidosis from poor tissue perfusion.
Positioning: If the patient is on the IABP, reposition him often and
perform passive range of motion exercises to prevent skin breakdown,
but don’t flex the patient’s “ballooned” leg at the hip because this may
displace or fracture the catheter.

58. DISCHARGE AND HOME CARE
GUIDELINES
Lifestyle changes must be made to avoid the recurrence of cardiogenic
shock.
Control hypertension: Exercise, manage stress, maintain a healthy weight,
and limit salt and alcohol intake.
Avoid smoking: The risk of stroke is the same for smokers and non-
smokers years after you stop smoking
Maintain a healthy weight: Losing those extra pounds would be helpful in
lowering the cholesterol and blood pressure.
Diet: Eat less saturated fat and cholesterol to reduce heart disease.
Exercise: Exercise daily to lower blood pressure, increase high-density
lipoproteins, and improve the overall health of the blood vessels and the
heart.

59. PROGNOSIS
Cardiogenic shock is the leading cause of death in acute MI. In
the absence of aggressive, highly experienced technical care,
mortality rates among patients with cardiogenic shock are
exceedingly high (up to 70-90%).
The overall in-hospital mortality rate for patients with
cardiogenic shock is 39%. For persons 75 years and older, the
mortality rate is 55%; for those younger than 75 years, it is
29.8%. For women, it is 44.4% compared to 35.5% in men.

60. SUMMARY

61. Intra Aortic Balloon Pump

62. INTRODUCTION
Intra-aortic balloon pump (IABP) remains the most widely used circulatory
assist device in critically ill patients with cardiac disease.
decrease
myocardial
oxygen
demand
increase
cardiac
output

63. PURPOSES
To stabilize the patient until
 Left ventricle recovers from acute injury
 Surgical correction of mechanical problems causing acute failure. eg:
ruptured ventricular septum.
 Heart transplantation
 Decision to place a device as “destination therapy”

64. INDICATIONS
Hemodynamic support during or after cardiac catheterization (21%)
Cardiogenic shock (19%)
Weaning from cardiopulmonary bypass (13%)
Refractory unstable angina (12%)
Refractory heart failure (6.5%)
Mechanical complications of acute myocardial infarction (5.5%)
Intractable ventricular arrhythmias (1.7%)

65. OTHER INDICATIONS
Bridging device for other mechanical support (VAD)
Support during transport
Cardiac support for hemodynamic challenged patients with
mechanical defects prior to valvular stenosis, papillary muscle rupture,
ventricular aneurysm.
Cardiac support following correction of anatomical defects

66. CONTRAINDICATIONS
Absolute:
Aortic valve insufficiency
Abdominal, aortic or thoracic aneurysm.
Relative:
End-stage cardiomyopathies-unless bridging to VAD
Severe atherosclerosis
End-stage terminal disease
Abdominal aortic aneurysm
Uncontrolled sepsis and coagulopathy
Uncontrolled bleeding disorder

67. BASIC PRINCIPLES OF
COUNTER PULSATION
Counter pulsation: Balloon inflation in diastole and deflation in early systole
Balloon inflation causes ‘volume displacement’ of blood within the aorta,
both proximally and distally
Potential increase in coronary blood flow and potential improvements in
systemic perfusion

68. IABP

69. GOALS OF INFLATION
Increase coronary perfusion pressure
Increase systemic perfusion pressure and peripheral oxygen
supply
Decrease SVR
Inflation of the IAB during diastole increases aortic volume and
pressure

70. GOALS OF DEFLATION
Decrease afterload
Decrease MVO2
Decrease assisted peak systolic pressure (APSP)
Increase cardiac output and ejection fraction (increase forward flow)
IAB deflation just prior to systole creates a potential space in the
aorta. This reduces aortic volume and pressure.

71. MECHANISM OF ACTION
It deflates in systole increasing forward blood flow by reducing after load and
actively inflates in diastole increasing blood flow to the coronary arteries.
These actions have the combined result of decreasing myocardial oxygen
demand and increasing myocardial oxygen supply.

72. COMPONENTS

73. IABP TIMING MODES
Automatic
• Tracks
cardiac
cycle,
cardiac
rhythm and
adjusts
automatically
Semi-
Automatic
• Operator
must adjust
inflation and
deflation
Manual
• Must adjust
inflation and
deflation
• Can set fixed
rate

74. IABP SIZING CHART

75. APPROACH AND
PLACEMENT
The balloon is situated 1-2 cm below
the origin of the left subclavian artery
and above the renal artery branches.
On daily X-ray, tip should be visible
between 2nd and 3rd ICS.

76. TRIGGER
This is the way the IABP identifies the beginning of the cardiac cycle.
ECG: Uses R wave on the ECG to initiate the pumping.
Pressure: The arterial pressure waveform is used to trigger.
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.

77. TRIGGER
The most commonly used triggers are the ECG waveform and the systemic arterial
pressure waveform.
The balloon inflates with the onset of diastole, which corresponds with the middle of
the T-wave.
The balloon deflates at the onset of LV systole and this corresponds to the peak of
the R-wave.
Poor ECG quality, electrical interference, and cardiac arrhythmias can result in erratic
balloon inflation.

78. AUGMENTATION
This is the ability of the balloon to be fully expanded and contain the full
amount of helium for the catheter.
When the balloon is rapidly inflated at the onset of diastole, an additional 35
to 50ml of volume is suddenly added to the aorta.
This creates an early diastolic pressure rise in the aortic root, increasing
coronary artery perfusion pressure.
Early diastolic pressure increase is referred to as the diastolic augmentation.

79. AUGMENTATION
The augmentation pressure
is the pressure generated
by the balloon when it
inflates during diastole.

80. FACTORS IMPACTING
AUGMENTATION
Physical
Position
Volume
Diameter
Occlusiveness
Drive Gas
Duration of Inflation
Efficiency of System
Arterial Pressure
Aortic Pressure / Volume Relationship

81. FREQUENCY (RATIO)
1:1
1:2
1:3

82. SETTING UP THE MACHINE
Ensure proper connections.
The battery can withstand pumping for approximately 24 hours.
Ensure both an ECG and pressure trace can be obtained from the
patient on the screen of the IABP.
Frequency when first commencing pumping is on 1:1.
Connect the extension tubing to the balloon catheter and on the
balloon console at the back.

83. SETTING UP THE MACHINE
Once connected, press the IAB fill button, holding it down for
a second.
A prompt on the screen will come up so you know it is filling.
Once filled, commence pumping by pressing the
assist/standby button.
 Then increase slowly the augmentation to maximum.

84. ARTERIAL WAVEFORM
A: Ventricular systole
B: Ventricular diastole
C: Dicrotic notch

87. DEFIBRILLATOR
The current IABP is completely isolated from the patient and
safe to have the patient defibrillated, ensuring staff remains clear
from the IABP when shock is delivered.

88. Trouble
Shooting

89. TROUBLE SHOOTING
No trigger – Reconnect the ECG leads or pressure cable.
IABP disconnected – Reconnect the extension tubing press IAB fill for 3
seconds till the prompt is on the screen.
Rapid gas loss – Inform physician. Check all the connections. Catheter
need to be removed and replaced. Check IABP catheter: examine the
catheter and extension tubing for any sings of kinking.
Low helium - Replace helium cylinder. Ensure that O ring is in place.
Low battery – Ensure that the balloon pump is connected to main
Augmentation below limit set – Review the alarm set and consider
lowering it in line with patient’s progress.

90. LOW PLATEAU PRESSURE
Low balloon volume
Too small of balloon
Balloon placement too low in
aorta
Decreased SVR (increased aortic
compliance)

91. BALLOON PRESSURE WAVEFORM
ARTIFACT
Balloon still in sheath
Suture too tight
Partial kink
Slow helium speed
Tortuous vessels

92. ELEVATED BASELINE
Kinked catheter
Partially wrapped balloon
Balloon in sheath
Overfill
Balloon too low in aorta
Balloon too large

93. BASELINE BELOW ZERO
Blood in tubing
Leak in tubing (helium loss)
Kinked catheter
Ectopy

94. SQUARE OR ROUNDED PLATEAU
(HIGH PRESSURE)
•Partially wrapped balloon
•Kinked catheter or tubing
•Balloon in sheath
•Too large of balloon
•Inaccurate balloon placement

95. WHEN TO DISCONTINUE
IABP?
If the following clinical picture is present,
• Signs of hypoperfusion due to low CO are absent.
• Urine output can be maintained above 30ml per hour.
• Need for positive inotropic agents is minimal.
• Heart rate is less than 100 beats per minute.
• Ventricular ectopic beats are < 6 per minute.
• Cardiac index remains equal to or greater than 2L/min/m2.
• Index of LVEDP does not exceed greater than 20% above
pre-weaning level.
• Absence of angina.

96. WEANING
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
Monitor patient closely If patient becomes unstable,
weaning should be immediately
discontinued
Decrease augmentation

97. IABP REMOVAL
Check platelets and coagulation factors
Deflate the balloon
Apply manual pressure above and below IABP insertion site
Apply constant pressure to the insertion site for a minimum of 30 minutes
Check distal pulses frequently

98. COMPLICATIONS
Vascular
Miscellaneous
Balloon
related

99. COMPLICATIONS
Vascular complications
Limb (and visceral) ischemia
Spinal cord ischemia
Renal ischemia
Vascular laceration necessitating surgical repair
Major hemorrhage from arterial dissection
Cholesterol embolisation is an infrequent occurrence that may
result in limb loss

100. COMPLICATION
Cerebrovascular accident is a rare complication
Sepsis is uncommon unless counterpulsation continues for more
than seven days.
Balloon rupture is an uncommon event, and is generally related to
the balloon pumping against a calcified plaque.
Rupture may be followed by thrombus formation within the balloon,
which may complicate removal
In order to prevent helium gas embolisation from the IABP, the
balloon console will withdraw helium from the balloon and shut down
the system with an alarm when it detects a loss of pressure.
Fall in platelet count, haemolysis, seromas, groin infection, and
peripheral neuropathy.

101. Nursing
Management

102. KEY NURSING
CONSIDERATIONS
Pressure assessment for optimization of therapy
Balloon mobility
Left radial pulse assessment
Urine output
Distal pulse assessment
Groin care
Platelets
Other complications

103. ASSESSMENT
Cardiovascular assessment include
Vitals signs
Cardiac output
Heart rhythm
Heart regularity
Heart ischemia
Urine output
Peripheral perfusion

104. NURSING DIAGNOSIS
Potential for decreased tissue perfusion in the lower extremities
related to possible catheter obstruction, emboli, thrombosis,
manifested by signs and symptoms of decreased perfusion in legs.

105. GOAL 1: MINIMIZE THE RISK OF DECREASED TISSUE
PERFUSION IN LOWER EXTREMITY
Record the quality of peripheral pulses before insertion of the IABP
catheter.
 Evaluate quality of peripheral pulses, skin color, capillary refill, and
temperature at least hourly.
Maintain the anticoagulation level at prescribed range by accurate
monitoring of heparin.
Assist the patient with ankle flexion and extension every 1-2hrs.
Maintain cannulated extremity in a straight position, avoiding hip
flexion.
If the patient is alert, instruct patient in importance of avoiding hip
flexion.
Maintain continuous alternating inflation and deflation of the balloon

106. NURSING DIAGNOSIS
Decreased cardiac output related to suboptimal IABP therapy,
manifested by lowered mean arterial pressure with requirement for
high dose inotropic support.

107. GOAL 1: TO PREVENT DECREASE IN CARDIAC
OUTPUT AS A RESULT OF SUBOPTIMAL IABP
THERAPY.
 Verify correct timing of IABP hourly. Make corrections as
needed.
Document settings for inflation, deflation and systolic, end
diastolic and mean arterial pressures with IABP assistance.
Document level of diastolic augmentation. Evaluate for a decrease in
augmentation.
Maintain proper volume of balloon to ensure optimal diastolic
augmentation.
Refill balloon every 2 to 4 hrs according to unit protocol, use automatic
filling mode if available.

108. GOAL 2: TO REDUCE OR ELIMINATE SITUATIONS THAT WILL
INTERFERE WITH MAINTENANCE OF PROPER IABP TIMING ASSIST
RATIO
Re -evaluate the timing anytime there is a greater than 10-20 beat change
in heart rate or onset of dysrhythmias.
Maintain adequate ECG trigger signals to IABP console.
Change any ECG electrodes that become loose, placing new ones on clean
,dry skin.
Notify physician of any dysrhythmias.
 Administer anitarrhythmic agents as ordered.
Maintain patient in proper body position( head of the bed 15 degree elevated and
no hip flexion).
Instruct radiologists and other personnel not to sit patient upright

109. CONCLUSION
Cardiogenic shock is a major, and frequently fatal, complication of a
variety of acute and chronic disorders, occurring most commonly
following acute myocardial infarction (MI).
IABP plays an important role in saving the life of patients. Careful
monitoring is of utmost importance as a nurse.

110. REFERENCES
Contemporary Management of Cardiogenic Shock A Scientific Statement From the American
Heart Association https://www.ahajournals.org/doi/pdf/10.1161/CIR.0000000000000525
Belleza M, RN. Cardiogenic Shock Nursing Care Management: Study Guide [Internet].
Nurseslabs. 2017 [cited 2019 Jan 15]. Available from: https://nurseslabs.com/cardiogenic-
shock/
Lawson WE, Koo M. Percutaneous Ventricular Assist Devices and ECMO in the Management of
Acute Decompensated Heart Failure. Clin Med Insights Cardiol. 2015;9(Suppl 1):41-8.
Published 2015 Apr 1. doi:10.4137/CMC.S19701
Woods Susan L. Cardiac nursing, Lippincott Williams & Wilkins, 6th edition, page no: 623-629,
633-634
Arrow educational material
Self-directed learning package: intra-aortic balloon pumping by Linda Williams
https://nurseslabs.com/cardiogenic-shock/
file:///C:/Users/hp/Desktop/Intra-Aortic_Balloon_Pump.pdf
https://www.mdpi.com/journal/reports-02-00019-v2.pdf/9
https://radiopaedia.org/articles/intra-aortic-balloon-pump?lang=gb