stroke volume (SV is dependent on preload, afterload and

contractility)
SV is measured by stroke distance x aortic root diameter
stroke distance (AUC) x HR, linear cardiac output parameter,
distance moved by a column of blood through aorta in 1 minute
(1200cm = high flow state)
corrected (systolic) flow time (FTc)
indicates preload
normal = 0.33-0.36s
interpretation of FTc and PV indicates afterload
peak velocity (PV)
indicates contractility
normal range is age related (20yrs 90-120 cm/sec, 90 yrs 3060 cm/sec)
interpretation of FTc and PV indicates afterload
heart rate

Pressure Monitoring Definitions

Zeroing
= a process which confirms that atmospheric pressure results in a
zero reading by the measurement system.
intermittent confirmation ensures the absence of
baseline drift where atmospheric pressure no longer
reads zero -> resulting in aberrant results
this is relatively common with disposable transducers
Levelling (or establishing the zero reference point)
= the process which determines the position on the patient you
wish to be considered to be zero.
transducers are placed at this point (often utilising fluid
filled tubing).
this is the level of the right atrium (midaxillary line in
the supine patient)
significant errors in measurement may occur if readings
using different zero reference points are used (ie. CPP)
Calibration
= the process of adjusting the output of a device to match a
known input value
verification of calibration requires the use of a gold
standard (ie. mercury or water manometer).
requires a two-step procedure (confirming that zero =
zero and 100mmHg = 100mmHg)
this assesses linearity of the system
the calibration of disposable transducers is preset and
cannot be altered.
Oesophageal Doppler
USES
non-invasive cardiac output monitor
Contra-indications
IABP
severe coarctation
known pharyngo-oesophageal pathology or injury
esphagectomy
severe bleeding
awake patient (relative)
Indications
major surgery with large fluid/blood shifts
high risk patients
haemodynamic instability
DESCRIPTION
measures blood flow velocity in the descending aorta using a
flexible ultrasound probe
measurement is based on the Doppler Principle: a doppler shift in
frequency occurs when the ultrasound wave is reflected back
from moving RBCs, with the shift in frequency proportional to
the velocity of the blood flow
measurement is combined with the cross-sectional area of the
descending aorta (using a nomogram based on age, weight and
height some models measure aortic root diameter using TOE)
probe contains crystals that produce a continuous ultrasound
wave of 4 MHz
single use, latex-free, silicone-based

METHOD OF INSERTION AND/OR USE

lubricate probe well & inserted via the nasal or oral route
advanced and rotated in the oesophagus (typically sits at level of
the 5th and 6th thoracic vertebrae where the aorta is adjacent and
parallel to the oesophagus)
some devices display the aortic pressure waveform allowing
confirmation of optimal probe position
turn volume up initially (sharpest sound = best position)
input age, height and weight
insert probe to 35-40cm from teeth (T5/6)
manipulate probe until characteristic Doppler signal found (well
defined triangle with black centre surrounded by red with white
in trailing edge) = distribution of RBC velocities at a given point
in time
adjust cycle length (5 = good starting point), gain (to decrease
ambient noise, start at 5 also)
the brighter (whiter) the colour the greater the number of RBCs
travelling at the given velocity
it is a dynamic monitor so needs refocusing prior to each reading
INFORMATION OBTAINED
Haemodynamic parameters:
cardiac output (Q = SV x HR)
Q is estimated by minute distance

types: Gaeltec pressure transducer, Ladd counter-pressure

transducer, Camino fiberoptic transducer, disposable extradural
sensor
METHOD OF INSERTION AND/OR USE
similar to an intraparenchymal monitor, but does not penetrate
dura (see Codman)
OTHER INFORMATION
Advantages
decreased risk of infection
COMPLICATIONS
Disadvantages
signal damping
cant aspirate CSF
underestimates high ICP
Transcranial Doppler (TCD) Ultrasound
TCD is a non-invasive technique for monitoring blood flow
velocity (FV) in the basal cerebral arteries using Doppler
ultrasound
USES
assessment of blood flow velocity through cerebral arteries is
useful for:
emboli
stenosis
vasospasm post SAH
assessment of cerebral blood flow
DESCRIPTION
pulsed Doppler probe -> graphs velocity over time

Actions from readings (need to be interpreted in clinical context)

low SV -> fluid
low FTc -> fluid
low PV -> inotrope
low PV + low FTc -> decrease afterload
PROS AND CONS
Advantages
minimally invasive
provides real time measurements
Disadvantages
learning curve (significant inter and intra-observer variability)
probe displacement requiring repositioning
difficult to use in an awake patient
Complications
esophageal bleeding, ulceration, or perforation
stricture formation
inaccurate measurements from probe displacement
OTHER INFORMATION
Doppler equation: Fd= 2FtVCos / C
where Ft is the transmitted Doppler frequency, V is the speed
of blood flow, Cos is the Cosine of the blood flow to beam
angle and C is the speed of sound in tissue
perioperative use in the UK is supported by NICE guidelines and
is embedded in enhanced recovery after surgery (ERAS)
programmes with financial incentives this based largely on the
surrogate outcome of reduced hospital length of stay
Extradural ICP monitors
USES
ICP monitoring
DESCRIPTION
catheter inserted though a burr hole but does not penetrate the
dura

METHOD OF USE
Technique
uses a 2 MHz probe (low frequency)
probe on temporal bone -> measure flow in MCA
phase shift is proportional to the speed of blood

during vasospasm there is an increase in flow velocity through

the narrowed segment that is proportional to the reduction in
vessel diameter.
Flow in MCA
normal flow: mean = 55cm/sec
mild: > 120cm/sec
moderate: > 160cm/sec
severe: > 200cm/sec
Lindegaard Ratio = mean velocity in the MCA / mean velocity in
ipsilateral extracranial internal carotid artery
high velocities in the MCA (>120cm/s) may be due to
hyperaemia or vasospasm.
the Lindegaard Ratio helps distinguish these conditions.
<3 = hyperaemia
>3 = vasospasm
-> 3-6 mild
-> >6 severe
OTHER INFORMATION
Interpreting flow
increases in flow velocity may be vasospasm or hyperaemia (to
differentiate compare flow through MCA with flow through
ICA)
reverberant flow (flow forward during systole and backward
during diastole) = no sustainable cerebral perfusion pressure
Advantages
non-invasive
quick and easily repeatable
performed at the bedside
can be used to monitor spasm post-treatment
Disadvantages
sensitivity 80% compared to angiography
operator dependent
por for distal vessels (i.e. other than MCA and ICA)
potential confounders include hypo/hypercapnia, hematocrit, BP
edema and vasopsam may be difficult to distinguish post-op
difficult views in some patients (e.g. thick skulls!)
Bispectral Index (BIS) Monitoring
BIS monitor was developed by Aspect Medical Systems
BIS = bispectral index
other depth of anaesthesia monitors exist (e.g. Entropy)
USES
used to monitor the depth of sedation or anaesthesia
DESCRIPTION
Sensor consists of disposable, wet gel electrodes
Cable
Monitoring module interfaces with anaesthesia machine or
monitoring systems
METHOD OF USE
best describe as a monitor of the depth of the hypnotic
component of anaesthesia
fronto-parietal application of electrodes
the monitor generates a number
100 = normal cortical activity (maximal laertness)
0 = cortical electrical silence
an EMG signal and Signal Quality Index is displayed as well as a
single channel EEG
The BIS algorithm
EEG data recordered from healthy adults who underwent
repeated transitions between consciousness and unconsciousness
using different anaesthetic regimens

analysis identified those features of EEG recordings that best

correlated with clinical depth of sedation/anaesthesia in
essence, the complexity of the EEG reduces with increasing
depth of anaesthesia
these were fitted to a model by multivariate logistic regression
the resulting algorithm generates a bispectral index (BIS)
it has been validated on healthy and now other patient
populations
COMPLICATIONS
Benefits
BIS < 60 results in very low levels of postop recall
shown to lower anaesthetic consumption
slightly quicker awaking
safe with diathermy and defibrillation
Problems
opioids produce changes in depth of consciousness not
discernable by BIS
BIS is not able to predict movement in response to surgical
stimulation
BIS values display incredible variability
not helpful when using N2O or ketamine
cannot use in children under 5
EVIDENCE IN ICU
low BIS associated with increasing delirium -> this can increase
morbidity and mortality
currently no high level evidence to guide use in ICU
possible role for patients who are paralysed in the titration of
adequate amounts of sedation and analgesia
may have an emerging role in out-of-hospital cardiac arrest
Increased Intracranial Pressure in Traumatic Brain Injury
normal ICP 7-15mmHg
sustained increases > 20mmHg is associated with ischaemic
brain injury
MONROE-KELLIE DOCTRINE
cranium can be thought of a fixed box such that any changes in
volume of its contents leads to an increase in pressure
contents: blood, CSF, brain tissue
CAUSES
artefact
coughing/valsalva
intracranial blood: haematoma (epidural, subdural, SAH,
intraparenchymal)
CSF: hydrocephalus
parenchyma: oedema, tumour, abscess
other: tension pneumocephalus
MANAGEMENT
exclude artefact/measurement errors
ensure adequate oxygen delivery
PaO2
treat clinically significant anaemia
maintain cerebral perfusion pressure to > 60mmHg (CPP = MAP
ICP)
fluids (avoid albuminSAFE TBI)
inotropes, vasopressors
optimise venous return from brain:
head up positioning, no venous obstruction (remove hard
collar), low PEEP
avoid cerebral vasoconstriction
PaCO2 35-40mmHg
decrease cerebral metabolic rate:
sedation, analgesia

paralysis
avoid hyperthermia
treat seizures
barbiturate coma
osmotherapies:
mannitol 0.25 to 1 g/kg, target Osm 300-320 mOsm/kg
hypertonic saline, target Na+ 145-155
Repeat CT scan to exclude a new mass lesion
Consider hypothermia (decrease cerebral metabolism, possible
neuroprotection)
Adverse outcome in paediatric TBI RCT from CCCTG
McIntyre MA suggesting titrated to ICP and prolonged
duration maybe beneficial
Ongoing trials including POLAR in ANZ
Consider surgical techniques (to reduce volume in the box, or
to open the box):
EVD (if already present, ensure patent and draining)
haematoma evacuation
decompressive craniectomy (controversial)
Decompressive craniotomy is contentious
DECRA showed decreased ICP and reduced ICU length of stay
but no mortality benefit and a greater number of patients with an
unfavourable neurological outcome in those who received
decompressive craniectomy
Patients with mass lesions(unless too small to require surgery)
were excluded
Only a single surgical intervention was used
Codman ICP Monitor
intracranial pressure monitor
aka bolt
USES/INDICATIONS
Suspected raised intracranial pressure
severe head injury
unable to monitor neurologically
GCS < 8 and abnormal CT
GCS <8 and normal CT with 2/3 of: age >40y, motor
posturing and SBP <90 mmHg
stroke
cerebral edema
hydrocephalus
hepatic encephalopathy
DESCRIPTION
strain gauge tipped catheter or fiberoptic device

METHOD OF INSERTION AND/OR USE

sterile technique
bolt through fronto-parietal suture-line, in line with pupil
zero at external auditory meatus
penetrates through dura into CSF or intraparencymally
held in place by bolt
OTHER INFORMATION

Interpretation of Waveforms
High amplitude of 50-100mmHg sustained for 15 min (A
waves) raised ICP
Saw tooth with small changes in pressure every 0.5-2 minutes
(B waves) poor intracranial compliance
Low amplitude oscillations up to 20mmHg for 1 min (C waves)
normal
Flat ICP trace compression or kinking of transducer
Rounded appearance of the waveform raised ICP
ADVANTAGES
easy to insert (can be done at bedside)
less invasive than EVD
more accurate ICP measurements than extradural bolt
produces high fidelity wave forms
small
DISADVANTAGES/ COMPLICATIONS
infection
transducer tip may rest on brain and obstruct
aspiration of CSF not possible
tends to under-read pressures > 20mmHg
intracranial transducer cannot be calibrated once in situ
baseline drift (especially after 5 days)
remember they dont give an indication of infratentorial pressure
no RCT evidence of benefit
External Ventricular Drain
ICP monitor than allows CSF drainage
USES
measurement and treatment of raised ICP
hydrocephalus of at risk of hydrocephalus following TBI
DESCRIPTION
gold standard of ICP measurement
catheter inserted in lateral ventricle at operation via a burr hole
passes through brain tissue
transducer is usually remote but catheter tip transducer also
available
zero level is the external auditory meatus

Components
Sampling port
Connector for transducer cable
Safety pin to attach to pillow
Filter
Transducer
Collection tubing
Collecting chamber
Level marker connected to chamber
Measuring column (in centimetres)
Collecting bag
METHOD OF USE

Attach flushed transducer to fluid-filled catheter do not inject

Set transducer to reference level (EAM or aortic root)
Attach drainage manometer and set at 10-20 cm H2O at level of
EAM
Monitor ICP continuously with intermittent drainage (hourly)
unless clinically indicated, for which drainage may be increased
in frequency or continuously
Septic surveillance of CSF daily ( or as per protocol)
OTHER INFORMATION
Interpretation of Waveforms
High amplitude of 50-100mmHg sustained for 15 min (A
waves) raised ICP
Saw tooth with small changes in pressure every 0.5-2 minutes
(B waves) poor intracranial compliance
Low amplitude oscillations up to 20mmHg for 1 min (C waves)
normal
Flat ICP trace compression or kinking of transducer
Rounded appearance of the waveform raised ICP

ADVANTAGES
gold standard
ventricular pressure considered more reflective of global ICP
than subdural, extradural or subarachnoid pressure
less prone to occlusion
allows therapeutic withdrawal of CSF
compliance can be measured
zero calibration
cheap
new devices are antibiotic impregnated to reduce the risk of
infection (e.g. Clindamycin/Rifampicin)
DISADVANTAGES/ COMPLICATIONS
more difficult to insert than a Codman
infection (ventriculitis)
haemorrhage
damage to brain
accidental venting of CSF
cannot be inserted in coagulopathy
no RCT evidence of benefit
Intra-Aortic Balloon Pump
Intra-Aortic Balloon Pump (IABP) or intra-aortic
counterpulsation device
the balloon is inflated during diastole to increase coronary
perfusion and then deflated during systole to decrease afterload
This aims to improve myocardial oxygenation, increase cardiac
output and organ perfusion with a reduction in left ventricular
workload
INDICATIONS
IABP is used as a supportive treatment tool in a clinical context
that will improve (bridging therapy) due to recovery or treatment
cardiogenic shock
post bypass
post MI

cardiomyopathy
severe IHD awaiting surgery or stenting
severe acute MR awaiting surgery
prophylactically in high risk patient pre-stenting/ cardiac surgery
miscellaneous (i.e. post myocardial contusion which is expected
to recover with time)
Intra-Aortic Balloon Pumps have also been inserted as a last
ditch measure to stop haemorrhage from the aorta or its branches
(e.g. massive GI haemorrhage)
CONTRAINDICATIONS
aortic regurgitation
aortic dissection
severe aorto-iliac or PVD
aneurysm or other anatomical disease of aorta
prosthetic aortic tree grafts
local sepsis
lack of experience with management
severe coagulopathy
not effective in a setting of a CI of < 1.2 and tachyarrhythmias
DESCRIPTION
The IABP has two parts:
(1) a large bore catheter with a long sausage-shaped balloon at
the distal tip, and
(2) a console containing a pump that inflates the balloon
balloon is made of a polyurethane membrane mounted on a
vascular catheter
various catheter sizes usually 7.5 F with the balloon size
chosen according to height (2550 cc)
may be sheathed or sheathless
some newer catheters have fibreoptics that assist pressure
waveform detection and timing
helium is used to inflate the balloon as its low viscosity means
there is little turbulent flow so the balloon can inflate fast and
deflate slowly. It is also relatively benign and eliminated quickly
if there is a leak or the balloon ruptures
when inflated the balloon occludes 80-90% of the aorta
INSERTION
Preparation
patient positioned supine
sterile technique (gowns, gloves, mask, drapes, sterile prep
solution)
check for bleeding diathesis and other complications
Method
fully collapse balloon applying vacuum with 60 ml syringe; some
kits require that the plunger is completely pulled out to achieve
this
percutaneous Seldinger technique or surgical
with or without sheath
access femoral artery at 45 degrees with needle
pass guidewire through needle and advance until tip is is in
thoracic aorta. Wire should pass very easily
pass sheath over wire in similar manner to insertion of PA
catheter sheath (sheath is not always used)
Pass balloon through sheath over guidewire and insert estimated
distance measure from sternal angle to umbilicus then to
femoral artery. Must be inserted to at least the level of the
manufacturers mark (usually double line) to ensure that entire
balloon has emerged from sheath
Balloon should be positioned so that the tip is about 1 cm distal
to the origin of the left subclavian artery
watch for loss of right radial pulse (too high)

Remove wire return of blood via central lumen confirms that

the tip is not subintimal and has not caused a dissection
Flush central lumen and connect to transducer to monitor intraaortic pressure (the outer lumen transmits helium gas to the
balloon)
Confirmation of position
Arterial balloon waveform and pressures shown on console
check for normal morphology and appropriate timing of
inflation and deflation in 1:2 augmentation ratio
Chest x-ray or fluoroscopy
confirms radiopaque tip lies in the 2nd intercostal spaces just
above the left main bronchus; lower end of balloon should lie
cephalad to the renal arteries
or TOE
direct visualisation 1cm distal to the left subclavian artery
USE
Triggering and timing
The balloon is timed to inflate and deflate in time with the
cardiac cycle
Triggers include:
ECG (using the R wave to identify the onset of systole); if SR
then deflation can be for a set time period, in AF the balloon
deflates when R waves are sensed
If paced then pacing spikes can be used to detect cardiac cycle
events
Arterial waveform (using the arterial upslope to designate
systole)
An internal trigger mode is available for asystolic arrested
patients
Optimising performance
correct position (balloon just distal to left subclavian artery, 2cm
above left main bronchus)
optimal balloon volume
balloon timing
inflation at onset of diastole and deflation prior to beginning of
systole (check in 1:2)
regular rhythm
timing: 1:1 inflation takes place at the dicrotic notch
slope of augmented diastolic wave form is straight and parallel to
the systolic upstroke
the augmented diastolic pressure should exceed non-augmented
systolic pressure
the end-diastolic pressure at balloon deflation is lower than
preceding unassisted end-diastolic pressure by 15 mmHg
the systolic pressure following a cycle of balloon inflation should
be lower than the previous unassisted systolic pressure by about
5 mmHg

Efficiency affected by
timing of inflation and deflation
assist ratio
heart rate (tachycardia > 130/min reduces benefit of IABP)
gas loss from balloon
CI of 1.2-1.4 required for IABP to be effective
COMPLICATIONS
During insertion
failure to advance catheter beyond iliofemoral system because of
atherosclerotic disease (common)
aortic dissection and arterial perforation may cause
retroperitoneal hemorrhage
malposition
accidental femoral vein cannulation and damage to local
structures
During use
thrombosis at the insertion site causing limb ischemia
peripheral embolisation and end organ ischaemia (e.g. limb
ischaemia with compartment syndrome, gut, kidneys and spine)
incorrect positioning with vascular occlusion (e.g. SCA, renal
arteries and other aortic branches)
infection
perforation
balloon rupture (look for presence of blood in the connecting
tubing)
gas embolisation
haemolysis and thrombocytopaenia
peripheral neuropathy
timing errors
During or after removal
haemorrhage particularly with the sheathed sets, consider
surgical repair of insertion sites in sheathed balloons
pseudoaneurysm
AV fistula
entrapment leading to inability to remove (may be due to small
performation allowing blood to enter balloon, may require
aortotomy)
OTHER INFORMATION
Catheter types
balloon size based on height (25-50cc)
sheathed or sheathless kits
new fibreoptic catheters that improve arterial pressure waveform
detection and timing
Anticoagulation
controversial if routinely required during first the 24 hours
low dose heparin infusion often prescribed; some units infuse
heparinised saline through the transducer set
Causes of decreased augmentation
balloon not needed any longer (myocardial recovery)
balloon rupture
distributive shock (sepsis)
Management of helium embolus
immediate cessation of counterpulsation
placement of the patient head down
IAB removal
Consider giving broad spectrum antibiotics as the gas chamber of
the balloon is not sterile
Weaning
should be considered when inotropic requirements are minimal
achieved gradually (over 612 h) reducing the ratio of
augmented to non-augmented beats from 1:1 to 1:2 or less (1:3

ratio is the same as no support) and/or decreasing the balloon

volume
balloon should never be turned off in situ except when the patient
is anticoagulated because of the risk of thrombus formation on
the balloon
ECMO
in centers that use VA ECMO the role of IABP is controversial
IABP may offer some additional support to a patient on VA
ECMO by assisting LV function or by providing more pulsatile
flow to improve coronary perfusion
overall it seems more likely that IABP will interfere with VA
ECMO function due to its position in the aorta, and further
contribute to the risk of lower limb ischaemia
EVIDENCE
IABP for myocardial infarction, cardiogenic shock and coronary
revascularisation
IABP-SHOCK II trial (2012) showed no 30 day mortality benefit
from IABP insertion for cardiogenic shock following MI when
early revascularisation was planned. See Cardiogenic Shock
Literature Summaries for more details on this article. A
subsequent paper showed that there was no mortality benefit at
12 months either.
Ranucci et al (2013) found that in patients undergoing
nonemergent coronary operations, with a stable hemodynamic
profile and a left ventricular ejection fraction <35%, the
preincision insertion of intra-aortic balloon pump does not result
in a better outcome.
Sjauw et al (2009) systematic review found that only low quality
observational studies support IABP use post-STEMI for
thrombolysis, not for PCI. There was no support from
randomised studies.
TACTICS trial (2005) was a small trial that showed no mortality
benefit for IABP in addition to thrombolysis for STEMI, but
there was a trend to improved Killip class in patients with severe
heart failure/ cardiogenic shock
The Randomised IABP study group trial (1994) found that
patients randomized to aortic counterpulsation following
revascularisation for MI had significantly less reocclusion of the
infarct-related artery during follow-up (median 5 days) compared
with control patients (8% versus 21%, P < .03).
Despite the paucity of evidence for cardiogenic shock
complicating MI, up until 2012, use of IABP for mechanical
assistance had a class IC recommendation in the current
European Society of Cardiology guidelines and a class IB
recommendation in the American College of
Cardiology/American Heart Association Guidelines.
Intra-aortic Balloon Pump
Q1. What is an intra-aortic balloon pump (IABP). How does it work
as a circulatory assist device?
The IABP has two parts:
1.
a large bore catheter with a long sausage-shaped balloon at
the distal tip, and
2.
a console containing a pump that inflates the balloon.
The balloon is designed to sit in the proximal descending aorta. It
comes in various lengths according to body height, with balloon
volumes of about 30-50 mL. The balloon is usually filled with helium
gas, and when inflated should fill up 80-90% of the aortic diameter.
The IABP works by inflating and deflating at different phases of the
cardiac cycle. Balloon inflation augments diastolic blood pressure and
balloon deflation decreases afterload during systole.

Normal IABP waveform (from DerangedPhysiology.com click

image for source)
Balloon inflation in early diastole (usually triggered by the R wave on
the ECG) increases diastolic blood pressure. This in turn increases
systemic perfusion and coronary perfusion (at least in the hypotensive
patient). Balloon inflation thus displaces blood both proximally and
distally. The increase in coronary perfusion increases myocardial
oxygen supply.
Balloon deflation occurs at the end of diastole resulting in a decreased
end diastolic blood pressure. This reduces the aortic pressure at the
start of systolic ejection, thus decreasing the afterload that the heart
has to pump against. This decreases myocardial oxygen demand and
improves systemic perfusion during systole.
This animation may help in visualising how the IABP works (bear
with the funky accent! you may need to increase the volume):
Q2. What are the indications for IABP use?
The IABP can be used whenever there is cardiac pump failure if:
it may resolve spontaneously, or
a corrective procedure is planned.
In other words, there has to be some hope of the patient being able to
survive without an IABP in the future.
Some situations where an IABP is used include:
Cardiogenic shock after coronary artery bypass grafting
(CABG) or acute myocardial infarction
unstable angina
Acute mitral incompetence
Planned cardiac transplant
ventricular arrhythmias refractory to conventional treatment
cardiotoxicity from poisoning, e.g. verapamil overdose
Q3. How is an IABP inserted and positioned?
IABPs are usually inserted using the Seldinger technique via the
femoral artery so that the tip of the catheter is advanced proximally
into the aorta. Fluoroscopy is not essential for insertion, so an IABP
can be placed emergently.
IABPs must be appropriately positioned: The balloon tip is
positioned just distal to the origin of the left subclavian artery, and the
entire balloon should lie above the renal arteries.
Here is a more detailed description of the steps involved in IABP
insertion as described by Charles Gommersall:
heparinise patient prior to insertion of catheter providing
there are no contraindications such as recent surgery.
prep skin
fully collapse balloon applying 30 ml vacuum with 60 ml
syringe
insert needle into femoral artery at 45 and pass it through
both walls of artery. Withdraw needle until strong pulsatile
jet of blood is obtained
pass guidewire through needle and advance until tip is is in
thoracic aorta. Wire should pass very easily

Complications can occur during insertion, while the IABP is in use,

during removal, or after removal.
During insertion
failure to advance catheter beyond iliofemoral system
because of atherosclerotic disease (common)
aortic dissection and arterial perforation may cause
retroperitoneal hemorrhage.
During use
Ischemia o ischemia of the lower limbs (up to 25% of all IABP
patients)
may occur while the IABP is in place, or hours after removal
due to thromboembolic showers
ischemia usually results from thrombosis at the insertion site
Can affect contra-lateral leg due due to cholesterol emboli
and thromboembolic showers from the balloon
Close neurovascular monitoring essential sensorimotor
loss generally mandates removal
Pulseless limb may need to be tolerated if IABP is lifesaving
o Visceral ischemia
o Spinal ischemia
Balloon rupture causing helium embolus
o this may be heralded by high balloon inflation
Q4. When is an IABP contra-indicated?
pressures.
Contra-indications include:
o The key indicator of balloon rupture is the presence of
Aortic insufficiency
blood in the connecting tubing.
Aortic dissection
o Management involves immediate cessation of
Patent ductus arteriosus
counterpulsation, placement of the patient head down
and IAB removal.
Severe peripheral vascular disease
o Consider giving broad spectrum antibiotics as the gas
Thoracic aortic graft <12 months old
chamber of the balloon is not sterile.
the patients cardiac index is too low for there to be a
Hemolysis and consumptive thrombocytopenia
clinical benefit from IABP assistance
Peripheral neuropathy
Q5. What are the determinants of IABP efficiency?
Catheter-related infection
IABP efficiency is determined by:
Small perforation in balloon membrane
Timing of balloon inflation and deflation
o this may allow a small amount of blood to leak into
balloon lumen.
Assist ratio (e.g. 1:1 balloon inflation and deflation on
o The blood is dessicated by the dry helium and forms a
every cardiac cycle provides greater circulatory assistance
hard pellet which may stop the balloon from being
than 1:2 or 1:4 balloon inflation and deflation on every 2nd
removed without surgical aortotomy.
or 4th cardiac cycle )
During or after removal:
Heart rate (efficiency is greatly decreased at heart rates
Haematoma
>130/min)
Pseudoaneurysm
Gas loss from balloon (balloon volume)
AV fistula
Minimum cardiac index of 1.2 1.4 L/min/m2 is required
for IABP assistance to be clinically beneficial
Entrapment of the IABP
pass sheath over wire in similar manner to insertion of PA
catheter sheath
pass balloon over guidewire through sheath. Must be
inserted to at least the level of the manufacturers mark
(usually double line) to ensure that entire balloon has
emerged from sheath
balloon should be positioned so that the tip is about 1 cm
distal to the origin of the left subclavian artery. If fluroscopy
is not available during insertion the distance from the angle
of Louis down to the umbilicus and then to the femoral
artery insertion site should be measured to approximate the
distance the balloon should be advanced and the position
should be checked on CXR
remove wire. Return of blood via central lumen confirms
that the tip is not subintimal and has not caused a dissection.
flush central lumen with heparin saline and connect to
transducer to monitor intra-aortic pressure (the outer lumen
transmits helium gas to the balloon)
monitor Doppler ankle pressures and compare with
preinsertion value
Note: once the balloon has been inflated, even if it is then deflated, it
must not be removed through the sheath for any reason the sheath
must be removed first.

Q6. How can IABP function be optimised?

Optimisation can be achieved by ensuring that:
inflation of the balloon occurs at the dicrotic notch (forming
the sharp V)
the slope of rise of augmented diastolic waveform is straight
and parallel to the systolic upstroke
the augmented DBP at balloon deflation exceeds or is equal
to end-systolic BP
the end-diastolic BP at balloon deflation is lower than the
preceding unassisted end-DBP by 15-20 mmHg
the assisted SBP (following a cycle of balloon inflation) is
lower than the previous unassisted SBP by 5 mmHg
Q7. What are the complications of IABPs?