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The intra-aortic balloon pump: a nursing care study

Article in British Journal of Cardiac Nursing · May 2012

DOI: 10.12968/bjca.2012.7.5.222

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Care Study

The intra-aortic balloon

pump: a nursing care study
Rosy Piper is Cardiac Clinical Practice Facilitator, The Heart Hospital, University College London Hospital NHS
Foundation Trust, 16-18 Westmoreland Street, London, WG1 8PH; Tracey Bowden is Senior Lecturer in Cardiac
Care, School of Health Sciences, City University London. Email: rosy.piper@uclh.nhs.uk

T
he devastating and life-threatening condition of
cardiogenic shock occurs in 5–8% of patients
hospitalised with ST-elevation myocardial infarction
(STEMI) (Reynolds and Hochman, 2008). Cardiogenic
shock is the leading cause of death in myocardial infarction
(Rull, 2011) and mortality rates for cardiogenic shock are
around 60% (Hochman et al, 2006). This care study
describes the nursing and medical care given to a patient
who was admitted with acute myocardial infarction (MI)
complicated by cardiogenic shock requiring an intra-
aortic balloon pump (IABP) for cardiac support. A
pseudonym has been used to maintain confidentiality
(Nursing and Midwifery Council, 2008).
Presentation
Maggie was a 76-year-old lady who presented at her local
accident and emergency department (A&E) with epigas-
tric pain and was discharged several hours later. She went
back to her GP that afternoon who referred her back to the
A&E with possible diabetic ketoacidosis. She was com-
plaining of ongoing epigastric pain. An eventual 12-lead
ECG showed ST elevation in the anteroseptal leads (V1–
V4) and she was given a loading dose of aspirin (300 mg)
and transferred to our hospital under the new NHS
London Cardiac and Stroke Network’s non-ST elevation
acute coronary syndrome protocol (South London Cardiac
& Stroke Network, 2010). On arrival, her 12-lead ECG
showed increased ST elevation in the anteroseptal leads,
up to 3 mm in V2 and V3 (Figure 1) indicating an antero­
septal STEMI.
Maggie has no previous known cardiac disease. She has
a history of previous hiatus hernia, anaemia and osteoar-
thritis, which makes her fairly immobile. She also has
hypertension, hypercholesterolaemia and poorly control-
led type II diabetes.
Her admission medications can be seen in Table 1. She
was not on any regular aspirin.
Other risk factors for heart disease included low activi-
ty/exercise as a result of her arthritis; high body mass
index (BMI) and central obesity; her age and possible fam-
ily history of heart disease. Maggie is a non-smoker and
does not drink alcohol.
Maggie lives alone and speaks little English, although
her daughters visit her daily and assist her with washing,
dressing, cooking and shopping. In hospital they were able
to translate for her.
At our hospital, her chest pain had become more severe:
she became tachypnoeic, hypoxaemic and she developed
pulmonary oedema; deep Q waves and up to 4 mm ST
elevation in anteroseptal leads (V1–V4). Her heart rate
(HR) was 130 beats per minute, sinus tachycardia, with

Abstract Table 1.
Cardiogenic shock is an uncommon but potentially fatal complication
of acute myocardial infarction and must be managed carefully to Medications on admission
maximise recovery and patient prognosis. Current guidelines aim to
Medication To treat
manage this by earliest possible revascularisation along with
potential mechanical interventions such as intra-aortic balloon pump Calcichew x1 once daily Hypocalcaemia
(IABP) therapy (and continuous positive airway pressure) and Paracetamol 1 g four times daily Osteoarthritis
pharmacological management such as intravenous diuresis, opiates, Ibuprofen gel 5% three times daily Osteoarthritis
vasodilators, inotropes and vasopressors.
Senna x 2 nightly Constipation
Nursing care of the patient with an IABP focuses on assessing the
patient’s cardiac output, assessing the efficacy of pressure Ferrous sulfate 200 mg once daily Anaemia
augmentation, observing for and managing any potential complications Hydroxocobalamin 1 m/ml Anaemia
of this invasive therapy and psychological and spiritual care of the injection as required
patient. Gliclazide 80 mg twice daily Type 2 diabetes
Key words Metformin 1 g three times daily Type 2 diabetes
w Acute myocardial infarction w Cardiogenic shock w Intra-aortic Sitagliptin 100 mg Type 2 diabetes
balloon pump (IABP) w Augmentation w Augmented pressures
Perindoprol 2 mg once daily Hypertension
Submitted for peer review 7 March 2012. Accepted for publication 19 March 2012.
Conflict of interest: None declared Simvastatin 40 mg nightly High cholesterol

222 British Journal of Cardiac Nursing May 2012 Vol 7 No 5


Figure 1: Maggie’s presenting 12-lead ECG. This shows normal calibration markers (25 mm/second; 1 cm = 1mv); sinus tachycardia,
130 beats per minute, with unifocal ventricular ectopics (complexes 6 and 14); ST-segment elevation in anteroseptal leads.
frequent ventricular ectopics and her systolic blood pres-
sure (BP) had dropped to 90 mmHg. She was awake, but
agitated. A chest X-ray showed evidence of pulmonary
oedema; an echocardiogram showed that her ejection
fraction was 12% and that all of the anterolateral myocar-
dium of her left ventricle was akinetic. Cardiac enzymes
(troponin T) were raised to 8.718 nanograms/mililitre
(normal: 0.00–0.09 nanograms/mililitre). She was display-
ing the signs and symptoms of acute anteroseptal MI,
complicated by cardiogenic shock (Table 2)
Management
The aim of managing cardiogenic shock is to diagnose,
prevent further ischaemia and treat the underlying cause
(Rull, 2011) as well as reducing mortality. Recent guide-
lines suggest that a combination of pharmacological and
interventional strategies should be employed to manage
cardiogenic shock. As a result of the seminal research
study on the management of cardiogenic shock—the
Should We Emergently Revascularize Occluded Coronaries
for Cardiogenic Shock (SHOCK) trial and SHOCK regis-
try (Hochman et al, 1999)—most guidelines (Anteman et
al, 2004; Scottish Intercollegiate Guidelines Network
(SIGN), 2007; Dickstein et al, 2008) recommended early
revascularisation and IABP therapy in patients with shock
secondary to acute MI. Other therapies recommended for
its management are:
ww Continuous positive airway pressure (CPAP) consid-
British Journal of Cardiac Nursing May 2012 Vol 7 No 5
Care Study
ered for patients with acute coronary syndrome and
pulmonary oedema with associated hypoxia (SIGN,
2007)
ww IABP therapy if pharmacological interventions fail to
raise the systolic BP or perfusion status of the patient
(Anteman et al, 2004; SIGN, 2007; Dickstein et al, 2008;
Kushner et al, 2009).
Table 2.
Signs and symptoms of cardiogenic shock
Airway and Hypoxaemia, high respiratory rate, use of accessory
Breathing muscles, cyanosis, arterial blood gases: high
lactate, low pH, crackles heard in lung fields,
pulmonary oedema
Circulation Hypotension, tachycardia, ischaemic ECG, anginal
symptoms, high CVP, presence of elevated cardiac
enzymes, peripheral vasoconstriction, peripheral
oedema, poor peripheral circulation (no pulses, pale
and cool, slow CRT), low or no urine output
Disability Reduced consciousness level, aberrant glycaemic
levels, nausea and vomiting, pain/anginal
symptoms
Exposure Skin cool, pale and clammy (especially peripheries)
CVP = central venous pressure CRT = capillary refill time
Adapted from Chen (2010)
223
Care Study

Table 3.
Management of cardiogenic shock secondary to acute myocardial infarction
Pharmacological Oxygen To correct hypoxaemia and reduce ischaemia
therapy Morphine To reduce pulmonary congestion, to ease angina
IV diuretics (furosemide, bumetanide) To offload severe fluid retention, including pulmonary
oedema
IV nitrate infusion (GTN)—if systolic BP is To reduce preload and workload of the myocardium
maintained > 90 mmHg
IV inotropes (dopamine, dobutamine, enoximone, To increase contractility, increase cardiac index and
levosimendan) cardiac output
IV vasopressors (norepinephrine)—if inotropes To increase systemic vascular resistance and thus
are insufficient preload, cardiac output and perfusion
Interventional Non invasive ventilation (CPAP) if pulmonary To increase pressure in lungs and force excess water
and mechanical oedema and subsequent hypoxaemia present back into bloodstream so oxygenation can take place;
therapy to aid oxygenation and therefore reduce ischaemia
Immediate revascularisation (primary To restore myocardial perfusion and reduce
percutaneous coronary intervention or emergency ischaemia/injury and subsequent cardiogenic shock
coronary artery bypass braft surgery) as quickly as possible
Intra-aortic balloon pump counterpulsation To increase myocardial oxygen supply and decrease
myocardial oxygen demand, thus reducing ischaemia
GTN = glyceryl trinitrate CPAP = continuous positive airway pressure
Anteman et al (2004), SIGN (2007), Dickstein et al (2008), Kushner et al (2009)

The management of patients with cardiogenic shock artery and obtuse marginal branch but the culprit lesion,
secondary to acute MI is summarised in Table 3. which had caused a sub-total thrombotic occlusion, was in
Maggie was taken to our catheter laboratory for emer- the proximal left anterior descending artery (LAD), which
gency angiography. She had disease in her right coronary was consistent with her 12-lead ECG.

Table 4.
IABP terminology
Assist ratio The assist ratio refers to the degree of support provided by the IABP. When the inflation–deflation cycle occurs
with every heart beat the assist ratio is described as 1:1. This is normally the level at which therapy
commences. When the inflation–deflation cycle occurs with every second heart beat the assist ratio is
described as 1:2. A 1:2 ratio is required to evaluate balloon timings and may also be used when the patient
is being weaned. A 1:3 ratio may also be used.
Trigger A trigger is a signal that the IABP uses to identify the beginning of the next cardiac cycle and includes:
wwECG: the trigger event being the R wave (this is the most common)
wwPaced (V or AV): the trigger event being the ventricular pacemaker spikes on the ECG. The patient must be
100% paced for this trigger to be effective
wwPaced (A): the trigger event is the R wave on the ECG; this is not a commonly used trigger
wwPressure: the trigger event is the systolic upstroke
wwInternal: this trigger is only used when there is no mechanical cardiac cycle (ie during cardiopulmonary
bypass or asystole)
When the IABP recognises a trigger event the balloon is deflated if this has not already occurred.
Weaning The level of circulatory support provided by the IABP may be weaned via two main methods: frequency
reduction or volume reduction.
wwFrequency reduction: the assist ratio is gradually decreased while haemodynamic effects are observed
wwVolume reduction: the volume of helium gas that inflates the balloon is gradually decreased. This method
could potentially increase the chance of clot formation in balloon folds
There is no direct evidence to suggest that either frequency weaning or volume weaning exhibits greater
success, both are offered as legitimate options for the withdrawal of IABP support
Lewis and Courtney (2006), Chen (2010)

224 British Journal of Cardiac Nursing May 2012 Vol 7 No 5

 Care Study

In the catheter laboratory, her LAD was reopened with

a stent after she was given an oral fast-acting antiplatelet
drug (prasugrel). She was loaded with heparin and
abciximab and given intravenous (IV) furosemide 60 mg
to offload the pulmonary oedema. An IABP was inserted
via her left femoral artery to reduce her afterload and
maximise coronary, cerebral and renal perfusion.
At the end of the procedure, Maggie’s BP was 95/50 mmHg
with an augmentation pressure of 110 mmHg. This gave her Y fitting
a mean arterial pressure of 84 mmHg (normal:
70–100 mmHg), an indicator of good tissue perfusion. The Stylet wire
IABP was set to be triggered by the ECG, as standard, and
was set at a ratio of 1:1 (Table 4).
She was taken back to the coronary care unit and the
plan was to keep the IABP in situ for about 12 hours; to One-way valve
maintain her on IV heparin infusion for the duration of
the IABP therapy; to finish the abciximab infusion (stop-

ANDREW BEZEAR
ping if bleeding) and check full blood count and coagula-
tion screen in accordance with the trust’s heparin and
abciximab protocols.

The intra-aortic balloon pump

The IABP is a catheter with a long, helium-inflated balloon. Figure 2. The intra aortic balloon pump in situ
This balloon is situated in the descending thoracic aorta,
inferior to the left subclavian artery ostium and just superior The balloon inflates at the start of diastole, which is sig-
to the renal arteries (Overwalder, 1999) (Figures 2 and 3). nified by the dicrotic notch on the arterial waveform, and

ANDREW BEZEAR

Figure 3. Relative position of IABP console. With the catheter in place, Maggie could only sit up to a maximum 45° angle

British Journal of Cardiac Nursing May 2012 Vol 7 No 5 225

Care Study
is the part of the cardiac cycle when the coronary arteries
fill with blood. Its inflation pushes the blood down the
coronary arteries, increasing coronary (and cerebral) per-
fusion resulting in decreased angina, decreased signs of
ischaemia on the ECG and a decrease in the frequency of
ventricular ectopics of ischaemic origin (Chen, 2010).
The deflation of the balloon occurs on the R wave,
which signifies ventricular depolarization and occurs just
before systole. This creates a sudden drop in pressure in
the aorta, which ‘sucks’ the blood down the aorta (and
better perfuses the renal, mesenteric and peripheral arter-
ies). This reduces the afterload so that blood is ejected into
a partially empty aorta (Lewis and Courtney, 2006).
Effective deflation also results in (Chen, 2010):
a) Normal arterial pressure waveform
dicrotic notch
b) Arterial pressure waveform from an IABP with a 1:2 assist ratio
3
2 primary goal of IABP is to increase myocardial oxygen sup-
5 ply and reduce myocardial oxygen demand (Krishna and
1 identifying and managing deterioration in her condition,
4
Key
unassisted pressures (without IABP)
balloon assisted pressures
1. Unassisted end-diastolic pressure
2. Unassisted systole; systole without a preceding IAB pumped beat
3. Balloon inflation; diastolic augmented pressure
4. Balloon deflation during end-diastolic pressure producing a low
pressure referred to as balloon-assisted end-diastolic pressure
(BAEDP)
5. Assisted systole; the pressure generated after a balloon inflation–
deflation cycle
When checking the IABP waveform ensure that:
Balloon inflates on dicrotic notch (start of diastole)
ww
Augmentation (IABP) pressure should always be higher than the
ww
patient’s systolic BP
Assisted aortic end-diastolic BP should be lower than unassisted
ww
aortic end-diastolic BP
Assisted systolic BP should be lower than unassisted systolic BP
ww
Figure 4. Arterial pressure waveforms with and without IABP
augmentation
226
ww Improved forward flow
ww Decreased preload
ww Increased cardiac output
ww Improved urine output
ww Improved peripheral pulses and warm skin temperature
ww Decreased heart rate.
This dual action of increased coronary artery perfusion
and reduced afterload improves the supply/demand
imbalance.
The arterial waveform can be seen in Figure 4a. The
dicrotic notch signifies the closure of the aortic valve and
is the true beginning of diastole. Thus the IABP balloon
would inflate at this point, creating a second peak as the
balloon’s inflation creates a pressure surge. The IABP pres-
sure waveform has two peaks (Figure 4b). The first peak is
the patient’s own systolic BP. If the patient’s heart is being
well assisted by the IABP therapy, his/her systolic BP will
be lower than usual. The augmentation (IABP) peak
should exceed the patient’s systolic BP. The peak of the
augmentation (IABP balloon’s) pressure will provide the
extra ‘push’ of perfusion to the coronary arteries and other
organs so the heart does not have to. When the IABP is
effective, the patient’s assisted end-diastolic BP should be
lower than his/her unassisted end-diastolic BP. This shows
that the reduction in afterload has been effective.
Nursing care of a patient with IABP in situ
The nursing care of a patient like Maggie requires a high
level of competence, training and skills (Catton, 2006). The
Zacharowski, 2009) and maximise organ perfusion.
Maggie’s immediate nursing goals include anticipating,
and identifying complications of IABP (Table 5) as well as
the psychological and spiritual care for Maggie and her
family (O’Donovan, 2011).
The trust clinical guidelines on the management of patients
with IABP indicate the need for careful monitoring of the
patient on a quarter-hour to half-hourly basis for the first 2
hours after insertion and subsequently on an hourly basis.
The nursing observations on Maggie sought to meet the
above aims and centre on observing for complications as
well as any deterioration in her haemodynamic status. It is
helpful to assess patients such as Maggie from head to toe,
in order to systematically make these assessments (Figure
5). Moreover, the IABP is thrombogenic. It is usually rec-
ommended to anticoagulate (usually with a heparin infu-
sion) (Krishna and Zacharowski, 2009). Care surrounding
continuous heparin infusion, such as regular checking for
signs of infection at the peripheral IV cannula site; 6–8
hourly activated partial thromboplastin time (APTT)
monitoring (or according to local protocol) (APTT is a
measure of clotting) and observation for bleeding prob-
lems or signs of heparin-induced thrombocytopoenia,
should also be carried out.
Other than assessing her for potential complications,
some assessment of the IABP machine should also be
British Journal of Cardiac Nursing May 2012 Vol 7 No 5
 Care Study

made (Table 6). It is important for the nurse caring for a
patient in Maggie’s position to be knowledgeable about
how to assess the augmented pressure waveform alongside
the patient’s cardiac output and perfusion status so that
the nurse can make a judgement about whether or not her
pressure is being optimally augmented and whether the
IABP is having the intended outcome and appropriately
enhancing tissue perfusion. The two different peak pres-
sures of the IABP waveform, however, sometimes cause
confusion about which pressures should be documented
and used to titrate vasopressors or vasodilators (Quaal,
2001). To make matters more confusing, a non-invasive
blood pressure machine will record the IABP augmented
pressure as the systolic value, which may give a misleading
view of the patient’s cardiovascular status. Our hospital’s
guideline requires that the IABP’s invasive blood pressures
are documented along with the mean arterial pressure and
non-invasive BP, to fully assess the patient’s arterial and
perfusion pressures.
If adequate perfusion is not being achieved, however,
this may be because a complication has occurred with the
IABP catheter or machine; or that it is simply not enough
to act as cardiac support. This therapy will need to be
reviewed by the medical team, as the risk of IABP therapy
complications may outweigh the benefits.
Psychological, educational and spiritual care of Maggie
and her family is integral to her care (Reid and Cottrell,
2005). After some discussion with her and her daughters,
it became clear that they thought that Maggie was on ‘life
support’ so evidently, effective, concise and sensitive com-

Table 5.
Risks and complications of IABP
Complication Recognition Action
Thromboembolus Signs of CVA (presyncope, syncope, facial droop, Treat as normal guidelines,
CVA, MI, peripheral weakness on one side, confusion), MI (onset of new chest consider removal of IABP
thromboemobolus, renal/ pain, new ECG changes, new rise in cardiac enzymes, i.e.
mesenteric embolus troponin T/I) peripheral thromboembolus (sudden loss of
peripheral loss of circulation), possible APPT < 2
Aortic dissection Haemodynamic signs of haemorrhage, drop in Hb, Stop and remove IABP, urgent
Descending aorta sudden, severe chest or back pain, global myocardial aortic repair surgery,
ischaemia, syncope; diagnosed by TTE, cardiac MRI, CXR replacement of blood and
blood products
Balloon rupture Loss of pressure augmentation, backflow of blood into the Turn off IABP and remove;
Blood leakage, helium IABP tubing re-insert new IABP if still
dissipation into arterial indicated
bloodstream, loss of
augmentation
Balloon migration Upwards: occlusion of L subclavian artery and carotid Re-siting of balloon under
Upwards or downwards artery (loss of L arm circulation, loss of consciousness) fluoroscopy and securing with
Downwards: occlusion of renal & mesenteric arteries sutures/dressings; careful
(drop in urinary output, abdominal pain and swelling). monitoring for signs of further
Loss of pressure augmentation, diagnosed by CXR balloon migration
Femoral arterial complications Bleeding out of the insertion site or into the peritoneum Removal of IABP, pressure on
Bleeding (including retro- (lower back pain), haematoma around the insertion site, bleeding artery/haematoma,
peritoneal), haematoma, other signs of bleeding (drop in Hb, hypotension & surgical repair of femoral
occlusion of femoral circulation/ tachycardia), loss of perfusion to affected limb; numbness artery, replacement of blood
nerve of affected limb, vaso-vagal and blood products
Thrombocytopoenia Low platelet count, bleeding/bruising Remove IABP and heparin
Heparin induced infusion, replace platelets as
needed
Infection/sepsis Pyrexia, raised CRP and WBC, presence of heat, swelling, Potential removal of IABP,
Due to foreign body in pus around the insertion site, signs of sepsis antimicrobial therapy,
circulation up to 72 hours antipyretics, further monitoring
for infection signs
CVA = cerebrovascular accident MI = myocardial infarction APPT = activated partial thrombin time 
Hb = haemoglobin MRI = magnetic resonance imaging CXR = chest X-ray 
CRP = C-reative protein WBC = white blood cell count
Adapted from Catton (2006), Maquet (2009a, 2009b), Chen (2010)

British Journal of Cardiac Nursing May 2012 Vol 7 No 5 227

Care Study

Head Assess for signs of CVA (thromboembolus), or lowered GCS

or confusion (reduced CO, loss of augmentation, migration of IABP
balloon upwards, occluding the carotid artery) Airway/breathing Assess airway patency (syncope), and breathing
status: respiratory rate, SpO2, breathing quality, breathing sounds,
pH, pCO2 and pO2 (pulmonary oedema, hypoperfusion and
subsequent acidosis, respiratory depression due to opiates)
Chest/back pain (and ECG) Assess for signs of new
chest pain/angina (MI/coronary thromboembolus,
loss of coronary perfusion, new ischaemic changes)
and back pain (aortic dissection)
Peripheral cannula Assess VIP score for patency &
infection status of the peripheral cannula; heparin infusion
should be running continuously according to prescription/
Peripheral radial circulation assess for signs of loss protocol; check APPTr to ensure levels are between 2–3
of radial circulation (peripheral thromboembolus)
especially in left arm (migration of IABP balloon,
occluding left subclavian artery): Feel pulse,
temperature, colour, movement and sensation of limb,
Abdomen assess for signs of abdominal
capillary refill time (CRT)
tenderness, pain or swelling (migration of
IABP balloon, occluding the mesenteric
arteries)
Groin site/femoral artery Assess for signs of
bleeding from site (bleeding / oozing around
puncture site, haematoma, retroperitoneal bleed
(lower back pain, reduced Hb) and infection of
Urinary output assess hourly urinary output
puncture site (heat, swelling & redness, pain or pus
(patient should be catheterised for accurate
at puncture site, pyrexia, raised CRP/WBC), check
urinary output measurement) for signs of
wound dressing (replace if soiled, not intact or signs
drop in cardiac ouptut, IABP balloon
of infection),
migration, occluding the renal arteries.
Record accurate fluid balance, to monitor for
Peripheral pedal circulation assess for signs of loss of pedal signs of circulatory overload/dehydration
circulation (peripheral thromboembolus) especially in limb with
IABP balloon inserted in it (migration of IABP balloon
downwards, occluding iliac/femoral artery, bleed or haematoma
occluding artery of affected limb): Feel pulse, temperature,
colour, movement and sensation of limb, CRT.
Look for evidence of compartment syndrome (swelling, pain,
hardness of tissues in legs)
istockphoto.com/colematt
Figure 5. Head-to-toe assessment of the patient on IABP

Table 6
Assessment of the IABP monitor and console

Monitor checks
Arterial pressure waveform wwAnalyse arterial waveform to judge whether pressure is being accurately augmented
wwTiming should also be assessed—this is usually achieved by reducing the frequency to
1:2 and freezing the screen
wwPressures should be checked (as in Figure 4) and inflation should correspond with the
dicrotic notch
wwCheck IABP frequency is 1:1 (every heartbeat is augmented) or as prescribed
ECG trace Check trigger is as prescribed (usually prescribed as ECG)
Augmentation gauge Check augmentation (balloon filling) is maximum
Helium tank indicator Check helium is full
Console checks
Trigger panel Check trigger is as prescribed
IAB frequency panel Check IABP frequency is as prescribed
Augmentation panel Check augmentation (balloon filling) is maximum

228 British Journal of Cardiac Nursing May 2012 Vol 7 No 5


munication about IABP and its role is important for these
patients. Plenty of reassurance, but honest and sensitively-
given health/illness and risk factor education (translated
by her daughters) facilitated her motivation to attend car-
diac rehabilitation and her understanding of what had
happened to her.
Other nursing priorities included assessing her for
signs of skin breakdown at her pressure areas and risk
assessment for venous thromboembolism due to her
immobility; assessing, recording and managing her
nutritional and hydration status and ensuring her blood
glucose levels were under control. Thus, an insulin slid-
ing scale was set up and she was put on a pressure-reliev-
ing mattress and assessed for pressure ulcers on a regular
basis. As Maggie would be connected to the IABP
machine and IV heparin infusion and she would need to
sit up no further than 45 degrees, help would need to be
given to her for any activities of living.
Maggie recovered well from her acute MI and shock and
the next day her IABP was successfully weaned then
removed by the medical staff when her activated clotting
time was <150 (levels may vary therefore it is important to
refer to local policies). When she was ready, she was dis-
charged home the following day on aspirin, clopidogrel (for
only 12 months) and a beta-blocker, which were added to
her existing statin, angiotensin-converting enzyme inhibi-
tor and other medications. She would be brought back in
1–2 months for percutaneous coronary intervention (PCI)
to her proximal right coronary artery and obtuse marginal
branch and would be followed up as an outpatient by the
cardiology team and cardiac rehabilitation service.
Conclusions
Cardiogenic shock is an uncommon but potentially life-
threatening complication of acute MI (Reynolds and
Hochman, 2008; Rull, 2011). Central to Maggie’s survival
in this instance was quick reperfusion of her myocardium
via emergency PCI, fluid offloading and appropriate car-
diac support—namely IABP therapy.
Nursing Maggie after these immediate life-saving inter-
ventions had been implemented focused on ensuring that
she had adequate cardiac output and checking that there
were no complications occurring with this invasive IABP.
One way for this to be done is regular head-to-toe checks,
which also incorporate assessment of the altered arterial
waveform and IABP machine itself. Holistic care should
be provided to serve the psychosocial and educational
needs of Maggie and her family, and to help her cope with
what has happened to her.
Aggarwal S, Slaughter MS (2008) Acute myocardial infarction compli-
cated by cardiogenic shock: role of mechanical circulatory support.
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Guidelines for the management of patients with ST-Elevation
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Cardiology / American Heart Association Task Force on Practice
Guidelines (Committee to Revise the 1999 Guidelines for the
Management of patients with Acute Myocardial Infarction).
Circulation 110:e82-292.
British Journal of Cardiac Nursing May 2012 Vol 7 No 5
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Care Study
Key Points
ww Understanding, assessing for and managing potential complications
of intra-aortic balloon pump (IABP) therapy is a cornerstone of patient
management
ww The nurse managing patients with IABP must accurately judge
whether IABP therapy is achieving good pressure augmentation
ww Psychological care and support, as well as health and illness advice
and education is important to help the patient and her family deal
with what has happened and will influence how empowered they are
in the future with their health choices
ww Patients on IABP therapy will need help with their activities of living
Catton J (2006) Intra-aortic balloon pump counterpulsation therapy
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the diagnosis and treatment of Acute and Chronic heart failure . (The
task force for the diagnosis and treatment of Acute and Chronic Heart
Failure 2008 of the European Society of Cardiology. Developed in
Collaboration with the Heart Failure Association of the ESC (HFA)
and endorsed by the European Society of Intensive Care Medicine
(ESICM). Eur Heart J 29: 2388–442
Hochman JS, Sleeper LA, Webb JG et al (2006) Early revascularization
and long-term survival in cardiogenic shock complicating acute myo-
cardial infarction. JAMA 295: 2511–5
Hochman JS, Sleeper LA, Webb JG et al (1999) Early revascularization in
acute myocardial infarction complicated by cardiogenic shock. SHOCK
Investigators. Should We Emergently Revascularize Occluded
Coronaries for Cardiogenic Shock. N Engl J Med 341: 625-34
Krishna M, Zacharowski K (2009) Principles of intra-aortic balloon
pump counterpulsation. Continuing Educating in Anaesthesia, Critical
Care & Pain 9(1): 24–8
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