Lillehei- Kalke valve (precursor of St.

Jude)

Cardiac Intensive Care Unit Management

Pt. comes from theatre
Monitor set up
Set up limits of HR, BP, CVP, Saturation, and Temprature.
Ventilator set up
Check for setting.
Action list in ICU
Examine pt.
Hemodynamics, Peripheral perfusion
Air entry, Heart sound & murmur.
Check-
ABG, Electrolytes, Hb-Hct
Chest X ray
Position of ET tube-Ideal between medial ends of two clavicles.
Position of NG tube.
Position of CVP line.
Position of chest drains.
Heart size.
Lung field-Collapse/Effusion/Pneumothorax/Congestion.
Order list
IV fluids
1 ml/kg/hr initially
2ml/kg/hr once peripheral temp >30degree
Usually 5% Dextrose / Ringer lactate unless C/I.
Antibiotics
Prophylactic antibiotic is administered for all Cardiac Surgery cases.
o Inj. Cefuroxime 50-100 mg/kg administered just before induction.

782
 o Repeat dose of Inj. Cefuroxime administered after 4 hours if surgery is
prolonged.
o Inj. Cefuroxime 50-100 mg/kg 8th hourly for 48 hours post- operatively (6
Doses).
o Antibiotic is continued for a patient for more than 48 hours if persistent fever
with elevated WBC counts.
o Inj. Amikacin 18mg/kg, once in a day for cases undergoing re-exploration,
along with Inj. Cefuroxime.
o If patient is reported to have a positive ET / Blood Culture, the antibiotic is
started according to the sensitivity report.
Antacid- Inj. Ranitidine
1mg/kg/dose x 12 hrly.
Digoxin 10 micgm/kg/d
Valves cases, PAH, TOF.
HR > 80/min & SR.
Used in fast JR.
Calcium & D 25% - Pt. < 10 kg
Calcium 3ml x 8hrly
D 25% 5ml x 8 hrly
Watch for
Heart rate ( Rhythm )
Blood Pressure.
CVP
Temperature Peripheral / Core.
Urine output.
Drainage.
ABGs & Electrolytes.
Hypokalemia
Ideally serum K to be kept around 4mmol/L.
(4.5 Pts K) x BW/4 = mmol/L/2= ml
0.3 x BW x (4.5-Pts K) = mmol/L/2 = ml
783
 Always under correct.
In renal failure According to Creatinine clearance
Hyperkalemia
K+ > 4.5mmol/L.
Check K+ every hourly.
Stop all K+ containing fluids (RL/FFP/Blood).
Correct metabolic/respiratory acidosis.
Calcium Gluconate 0.2-0.5ml/kg over 5 min.
Insulin 0.1 U/kg with 0.5 gm/kg of glucose.
Use Lasix if it persistently remaining high.
K Oxylate powder 1gm/kg 4th hrly through NG/PR.
Metabolic acidosis
0.3 x base excess x Body weight = ml of sodabicarb.
Quick calculation
o Base excess >5.0 7.5 -Pts wt = ml of sodabicarb
o Base excess > 7.5 1.5 times Pts wt.
Assessment of Cardiac output
Physical examination CO Normal CO

Peripheral perfusion Capillary filling Poor Good

(<3 Sec)

Core peripheral temp. Gr. > 3 degree < 3 degree

Peripheral pulses Impalpable/ weak Normal

Urine output <1 ml/hr >1ml/hr

784
Mental status CNS Disoriented Co-operative

Arterial pressure wave Small area under Large area under curve
curve Dicrotic notch occurs
Dicrotic notch later
soon after peak

Metabolic acidosis Base excess > -5 mmol/L < -5mmmol/L

In ICU setting
Parameters CO Normal CO

Heart Rate Tachycardia Normal HR

Blood pressure Low Normal

CVP High/Low Normal range

785
Peripheral temp Cooling Warm
( > 30 degree)

Urine output < 1ml/kg > 1ml/kg

Low Cardiac output

Rule out
o Cardiac tamponade (CxR , Echo )
o Pneumothorax ( Clinical , CxR)
Volume required
o Use blood if Hct is < 33
o Otherwise Haes 3%
Albumin 20% 100 ml in RL

Low CO

Adequate preload Inadequate preload

Increase/Add Inotropes Give
colloids

Reassess preload
Keep LAP 5-10mmHg or CVP 4-6mmHg.

Inotropes

786
 Infusion rate Mic/kg/min Indication
Starting dose

Dopamine - Mild/mod myocardial dysfunction

5 (5 - 20) st
- Use 1 .
- Renal vasodilatation
- If dose >15mics/kg/min consider adrenaline

Dobutamine -Mild-mod myocardial dysfunction with labile

5 ( 5 20) pulmonary vasculature.
-Vasoconstriction & Tachycardia to be avoided.
-Expensive.

Isoprenaline -Relative bradycardia/AV block.

0.05 ( 0.01 - 0.5) -Isoprin is a potent vasodilator & may be poorly
tolerated in patients with low coronary perfusion
pressures.

Milrinone - Inodilator.
50mic/kg loading dose - Beneficial effect on RV dysfunction.
(0.5-0.75mics/kg/min) - Hypotension & thrombocytopenia.

Dose calculation
ml/hr = Wt (Kg) x Dose (mcg/kg/min) x 60min
------------------------------------------

787
 1000 x Drug conc. (mg/ml)
Digoxin
Inotropic-Bradycardiac.
Uses
- Volume overloaded heart-ASD/VSD/AVCD
- PVH MS/MR
- CHF with tachycardia.
0.03mg/kg/24hrs Digitalizing dose.
0.01mg/kg/24hrs - Maintainace dose.
Care Should not be given if S.K+<4.0mmol.
HR < 100/min, Renal impairment, Digoxin toxicity (Ventricular ectopics,
AV block).

Ventilation & Respiratory support

Factors affecting post- op pulmonary function
Perioperative factors
-CT surgery causes VC, FRC small airway closure during tidal
ventilation-Intrapulmonary shunting-Needs oxygen.
-CPB results in extra vascular lung water- Lung compliance.
-Pain contributes to respiratory dysfunction.

-Drugs-Anaesthesia, Analgesia, Sedatives-Somnolence- Respiratory

depression
Pre-operative factors
-Airway problems.
-Parenchymal lung disease.
-Effect of cardiac lesion Pulmonary oedema.
PEEP
FRC & improves oxygenation.
Applied in most cases 4-5cms.
788
 Higher level of PEEP useful in
o Post perfusion wet lung.
o Pulmonary oedema.
o Lobar collapse.
o Tracheo-bronchomalacia.
o Excessive mediastinal bleeding.
C/I Hypovolemia & Fontan Operation.
After connecting pt. on Ventilator Check
Chest is moving.
Air entry on both sides is equal.
Oxygenation- Colour of lips & skin,SpO2
Check for O2 inlet is properly pushed or not.
Ventilator is achieving the set parameters.
ABGs
- 15 min after shifting & connecting to ventilator
- 1 hour after resetting the parameter
- 6th hrly on operative & 1st po day
Chest X-ray.
When to do Chest X-Ray
When pt. comes to ICU.
1st Po day morning for all open hearts.
Ventilation or oxygenation deteriorates
- To detect
1. Pneumothorax.
2. Pleural collection.
3. Lobar collapse.
4. Pulmonary oedema.
5. Position of ET tube.
Pt. gets reintubated.
Weaning from ventilator

789
 Routine
1. Stable hemodynamics with modest inotropic support.
2. Peripherally warmed up (>30 degree)
3. Good ABGs on FiO2 - 40%.
4. Normal peak inspiratory pressure (<25cm H2O).
5. Wide awake with good respiratory rate.
6. No major bleeding
7. No major neurological deficit or residual pharmacological impairment
of consciousness.
8. Good CxR
No parenchymal pathology.
No fluid (in or out of lung)
Long term Ventilation
1. No signs of chest infection or other major sepsis.
2. Adequate nutritional state.
3. Able to tolerate weaning without resort to excessive sedation.
4. Should tolerate T Piece trial.
RR < 25 ideal, < 30 Acceptable
PCo2 between 30-40
PO2 > 80-85
5. Weaning down to CPAP may take several days if lung compliance is
poor.
6. Never ignore Ventilatory alarms.
ET suction
Immediately after receiving in ICU.
Every 4th hrly.
If Blood tinged secretion
Use normal saline to clear blood.
Use 1:10 / undiluted adrenaline.
Frequent suction to clear the blood.
790
 If thick secretions Nebulize & put normal saline to clear the secretion.
High PCO2
Check ventilatory parameter.
Increase rate & MV.
Remove BVF from inspiratory limb & put on expiratory limb.
Check for thick secretion.
Check for Blood in ET.
Low PO2
Check FiO2.
Check inlet of O2 port.
Hyperinflate lung & see for SpO2 ing/not.
Check for thick secretion.
Check for blood in ET.
Extubation
Ability to breath satisfactorily on CPAP prior to extubation.
Routine cases 30 minutes.
Long term ventilation longer time with rest on pressure support
overnight.
For pediatric cases < 20 Kg give Hydrocortisone (2-4 mg/kg) &
Dexamethasone (0.25mg/kg/dose) 15-30 min before extubation.( To
avoid stridor)
Fast track for pediatric patients.
Post Extubation
Keep O2 on 6 L mask.
Check ABG after 1 hour.
Reduce O2 to 2 L if PO2 is >120.
Keep off O2 after 2-3 hours.
Need of O2 for longer time CABG/TOF.
Post Extubation Stridor
Give Hydrocortisone & Dexamethasone.
791
 Dexamethsone (0.25mg/kg/dose)6hrly with Ranitidine.
Oxygen
Recemic epinephrine Nebulization.
Or
2ml neat 1:1000 adrenaline Nebulization.
If resolution does not occur reintubate.

Fever
First 24 hours
Stress response due to CPB & Surgery
Causes
Stress induced - Common
Sepsis - Unusual in early PO
Low CO - Peripheral Vasoconstriction with central pyrexia
Malignant Hyperpyrexia - Very rare
Up to 37.5-37.9 degree One / two spike
o Use fan / Paracetamol.
Continuous fever & > 38 degree
o Fan / Paracetamol
o Cold saline Lavage in RT
o Tepid sponging
o Cooling blanket if >40 degree
Continuous fever for >4-5 hrs Hemogram
Continuous fever with > 38 degree Blood culture.
Fever after 48 Hours
Must investigate for infection.
Neurological damage can cause Hyperthermia.
Investigations includes
o Hematology, Biochemistry, Urine C/S, Blood C/S, ET secretion C/S.
Antibiotics to be changed

792
Blood Loss
Surgical bleeding.
Bleeding due to coagulation abnormality
-Preexisting coagulopathy.
-Residual Heparin effect.
-Removal /consumption of coagulation factors.
-Platelet defects.
1-2ml/kg/hr for 1-2 hrs - should be alert.
>2ml/kg/hr Significant.
Surgically significant bleeding
Loss in Any
1 hour 10% of blood volume
2 hour 8% of blood volume
3 hour 6% of blood volume
Estimation of blood volume
85ml/kg in <10kg
80ml/kg in 10-20kg
75ml/kg in >20kg

Management of blood loss

Replace blood loss.
Check ACT (80-120).
If ACT >130 Protamine 1mg/kg.
ACT normal Hemostat ( Aminocaproic acid) 100 mg/kg
If only mediastinal tube draining - PEEP
One unit of warm fresh blood.
Hypotension
The following is an approach to managing the hypotensive patient;
1. Look at the recent hemodynamic parameters.
793
2. Assess the cardiac output/index. Is this a "pump" problem? Or is it due
to low SVR?
3. Look at the cardiac rhythm.
4. Look at the CVP to assess preload.
5. Is the afterload high?
6. Is contractility decreased?
7. Is this tamponade? Is this an acute graft occlusion or spasm? Is this an
acute dehiscence of a valve repair?
Look at the recent hemodynamic parameters obtained from the Swan-
Ganz catheter.
Obtain another set as soon as possible if they have not recently been
done or if there has been a sudden change.
Assess the cardiac output/index.
If the cardiac index is in the normal range or high, then the patient does
not have a significant "pump" problem and the cause of the hypotension
is secondary to diminished peripheral arterial tone (low SVR). A
vasopressor agent should be considered.
The differential diagnosis of low SVR includes;
o SIRS - a proportion of patients post CPB will have significant
cytokine increases
o Sepsis
o Anaphylactic or anaphylactoid reactions including protamine
reactions,
o Drug-induced, toxicological - nitrates, antihypertensives, narcotics
and sedatives, etc
o Adrenal insufficiency (Was the patient steroid dependent pre-
operatively?)
o Hyperthyroidism, hypothyroidism,
o Neurogenic (spinal) shock

794
 If the cardiac index is low (< 2.0 to 2.2 L/min/m2) then the cause of the
hypotension is inadequate flow or a "pump" problem.
Look at the cardiac rhythm. Absolute or relative bradycardias or
tachycardias (commonly new atrial fibrillation) can lead to decreased
C.O. and should be corrected.
Look at the CVP to assess preload. A patient with a low C.I. and a CVP
that is "relatively" low should be given a fluid challenge.
Volume required
o Use blood if Hct is < 33
o Otherwise Haes 3%
Albumin 20% 100 ml in RL

Low CO

Adequate preload Inadequate preload

Increase/Add Inotropes Give
colloids

Reassess preload
Keep LAP 5-10mmHg or CVP 4-6mmHg.
High afterload. Secondary to vasoconstriction and hypertension.
Decreased contractility. This should be managed with inotropic agents
while simultaneously looking for the cause.
o Low pre-operative ejection fraction
o Prolonged CPB time or cross-clamp times, difficulty with
myocardial protection intra-op
o Acute bypass graft occlusion (check the ECG)
o Graft spasm (especially LIMA) - check the ECG for ST elevation
Tamponade.
795
 Acute valvular regurgitation. A valve repair or replacement can rarely
have acute dehiscence. Check for a new regurgitant murmur and new 'v'
waves on the PCWP tracing in the case of a MVR.
Management
Head low position.
Inj. calcium to be given 500mg.
Check
- Support lines are Ok.
- Support not changed recently.
- Arterial line position.
- CVP.
If CVP low give volume.
Purge 0.1 ml of support.
Adrenaline 1:10 dilution 1ml.
Add support if required.
Hypertension
Check with NIBP.
Check support line.
Increase NTG.
Add Nitroprusside.
Give Captopril 0.1mg/kg/dose-1mg/kg/dose.
Maintain intravascular volume.
VPCs/ Tachyarrhythmias
Check Electrolytes K+
Give Magnesium 0.5%W/V 0.2ml/kg.
Give Xylocard 1mg/kg then 15-50 micgm/kg/min.
Care during Xylocard
Give Amiodarone 5mg/kg then 5-15micgm/kg/min.
Care during Amiodarone
Bradyarrhythmias
796
 Check
Electrolytes, Rhythm, Pacemaker
Give Atropine
Give Salbutamol Nebulization.
Start Isoprenaline.
Broad QRS complex Hemodynamically unstable Pacing wires are there-
Start pacing.
Tamponade
Cardiac tamponade is compression of the heart that impairs ventricular filling
and leads to a low cardiac output.
The incidence of cardiac tamponade post-cardiac surgery has been reported to
be as high as 3 to 6 %.
The presentation of tamponade can be variable and requires a high index of
suspicion.
No single bedside test or finding is sensitive or specific enough to absolutely
rule in or out tamponade.
A "typical" presentation would be a patient who had initially excellent
hemodynamic parameters, bled from the mediastinal tube moderately, then the
bleeding "stopped" or blood ceased to drain from the tubes. (Always check to
make sure the tubes are not obstructed).
This is followed by hemodynamic deterioration with tachycardia, declining
cardiac output and stroke volume, and decreasing mixed venous oxygen.
The urine output typically decreases and other signs of end-organ
hypoperfusion develop including CNS changes and acidosis.
1. Search for alternate explanations for the low cardiac output (i.e.,
hypovolemia, myocardial ischemia, etc.).
2. Assure patency of the tubes.
3. Look for "equalization" of central pressures. In "classic" cardiac
tamponade, the pericardium is intact and the raised pericardial
pressures are transmitted equally to all four cardiac chambers. This

797
 results in an elevation and equalization of the CVP, PCWP, and PAD
associated with low CO. (CVP=PCWP=PAD).
4. In the post-op cardiac surgery patient, it is possible to have a small, well-
localized clot that impedes filling to only one chamber and thus cause
unequal pressure changes. For example, a right sided clot may raise only
the CVP and impair filling to only the right atrium or ventricle.
5. Low voltages on the ECG or an increase in the width of the superior
mediastinum on serial chest X-rays are generally poorly sensitive or
specific. They are rarely helpful.
6. Echocardiogram. This is the best test to assess for tamponade. Often a
trans-esophageal Echo (TEE) will be required because of poor "windows"
common in the post-operative state with Trans-thoracic echo (TTE).
7. The only treatment for cardiac tamponade
o Return to the OR,
o Re-sternotomy, and
o Evacuation of the clot with hemostasis of any ongoing bleeding.
o Volume resuscitation, inotropes, and vasopressors are temporizing
measures only in this situation.
8. If a patient with suspected tamponade suddenly deteriorates and
develops PEA (pulseless electrical activity)
o Urgent sternotomy should be done in the ICU.

Mechanical assist devices

Intra-aortic balloon pump
History
Kantrowitz described augmentation of coronary
blood flow by retardation of the arterial pressure
pulse in animal models in 1952.
In 1958,Harken suggested the removal of some

798
 of the blood volume via the femoral artery during systole and replacing it
rapidly in diastole as a treatment for left ventricular (LV) failure, so called
diastolic augmentation.
Moulopoulos and colleagues developed an experimental prototype of an
IABP whose inflation and deflation were timed to the cardiac cycle.
Bergman and colleagues described the first percutaneous insertion of
IABP.
The first prefolded IAB was developed in 1986.
Basic principles of counterpulsation
Counterpulsation is a term that describes balloon inflation in diastole and
deflation in early systole.
Balloon inflation causes volume displacement of blood within the aorta,
both proximally and distally.
This leads to a potential increase in coronary blood flow and potential
improvements in systemic perfusion by augmentation of the intrinsic
Windkessel effect, whereby potential energy stored in the aortic root during
systole is converted to kinetic energy with the elastic recoil of the aortic root.
Physiological effects of IABP therapy
Primary goal -> improve the ventricular performance of the failing heart
by facilitating an increase in myocardial oxygen supply and a decrease in
myocardial oxygen demand.
Aorta : Reduces systolic pressure, Increases diastolic pressure
Left ventricle: Reduces systolic pressure, Reduces end-diastolic pressure,
Reduces volume & wall tension
Heart : Reduces afterload, Reduces preload, Increases cardiac output
Blood flow : Increases coronary blood flow
IABP may also have favourable effects on right ventricular (RV) function
by complex mechanisms including accentuation of RV myocardial blood
flow, unloading the left ventricle causing reduction in left atrial and
pulmonary vascular pressures and RV afterload.

799
 IABP inflates at the onset of diastole, thereby increasing diastolic
pressure and deflates just before systole, thus reducing LV afterload. The
magnitude of these effects depends upon:
(i) Balloon volume: the amount of blood displaced is proportional to the
volume of the balloon.
(ii) Heart rate: LV and aortic diastolic filling times are inversely
proportional to heart rate; shorter diastolic time produces lesser balloon
augmentation per unit time.
(iii) Aortic compliance: as aortic compliance increases (or SVR decreases),
the magnitude of diastolic augmentation decreases.
Myocardial oxygen supply and demand
Inflation of IAB during diastole increases the pressure difference between
aorta and left ventricle, the so-called diastolic pressure time index (DPTI).
increase in coronary blood flow and, therefore, myocardial oxygen
supply.
Myocardial oxygen demand is directly related to the area under the LV
systolic pressure curve, termed as tension time index (TTI).
Balloon deflation during systole causes a reduction in the LV afterload,
thereby decreasing TTI.
the ratio of oxygen supply (DPTI) to oxygen demand (TTI), known as the
endocardial viability ratio (EVR), should increase if the IABP is working
optimally.
Coronary perfusion
According to the Hagen Poiseuille principle, flow through a tube is
directly proportional to the pressure difference across it and the fourth
power of the radius while being inversely proportional to the length of the
tube and the viscosity of fluid flowing through it.
Renal function

800
 Renal blood flow can increase up to 25%, secondary to increase in
cardiac output.
Decrease in urine output after insertion of IABP should raise the
suspicion of juxta-renal balloon positioning
Haematological effects
The haemoglobin levels and the haematocrit often decrease by up to 5%
because of haemolysis from mechanical damage to the red blood cells.
Thrombocytopenia can result from mechanical damage to the platelets,
heparin administration, or both.
INDICATIONS
Acute myocardial infarction
Refractory LV failure
Cardiogenic shock
Refractory ventricular arrhythmias
Acute MR and VSD
Cardiomyopathies
Catheterization and angioplasty
Sepsis
Refractory unstable angina
Infants and children with complex cardiac anomalies
Cardiac surgery : Weaning from cardiopulmonary bypass
Acute myocardial infarction
IABP is aimed at achieving haemodynamic stability until a definitive
course of treatment or recovery occurs. By decreasing myocardial work
and SVR, intracardiac shunting, mitral regurgitation, or both (if present)
are reduced while coronary perfusion is enhanced.
Severe mitral regurgitation secondary to papillary muscle dysfunction or
rupture after myocardial infarction can lead to significant haemodynamic

801
 instability. This can initially be managed by IABP, pending definitive
surgery.
Refractory ventricular failure
Can aid the progression to more definitive treatments such as ventricular
assist device or cardiac transplantation.
Cardiogenic shock
Class I indication (ACC/AHA guidelines) for the management of cardiogenic
shock not rapidly reversed by pharmacological therapy.
Unstable angina
Increased risk of developing acute myocardial infarction and death. By
improving the haemodynamic condition of these patients, IABP can facilitate
further percutaneous interventions or bridge the patient to surgery.
Cardiac surgery
Elective placement is considered in high-risk patients such as those with
significant left main stem disease, severe LV dysfunction (ejection
fraction, 30%), congestive heart failure, cardiomyopathy, chronic renal
failure, or cerebrovascular disease.
Weaning from cardiopulmonary bypass may be difficult in cases where
aortic cross-clamping is prolonged, revascularization is only partially
achieved, or pre existing myocardial dysfunction is present. Separation
from cardiopulmonary bypass may be marked by hypotension and a low
cardiac index despite the administration of inotropic drugs. The use of
IABP in this setting decreases LV resistance, increases cardiac output,
and increases coronary and systemic perfusion, facilitating the patients
weaning from cardiopulmonary bypass
CONTRAINDICATIONS
Absolute
Aortic regurgitation
Aortic dissection
Chronic end-stage heart disease with no anticipation of recovery
802
 Aortic stents
Relative
Uncontrolled sepsis
Abdominal aortic aneurysm
Tachyarrhythmias
Severe peripheral vascular disease
Major arterial reconstruction surgery

Technique of insertion and operation

The IABP device has two major components:
A double-lumen 8.09.5 French catheter with a 2550 ml balloon
attached at its distal end
a console with a pump to drive the balloon
Balloon is made of polyethylene and is inflated with gas driven by the
pump.
Helium is often used because its low density facilitates rapid transfer of
gas from console to the balloon. It is also easily absorbed into the blood
stream in case of rupture of the balloon.

803
 Before insertion, the appropriate balloon size is selected on the basis of
the patients height (as supplied by Datascope, for a patient, 152 cm in
height, a balloon volume of 25 cc is appropriate; for height between 152
and 163 cm, balloon volume 34 cc; for height 164183 cm, balloon
volume 40 cc, and for height .183 cm, balloon volume 50 cc). Smaller
balloons are available for paediatric use.
The diameter of the balloon, when fully expanded should not exceed 80
90% of the diameter of the patients descending thoracic aorta.
The IABP catheter is inserted percutaneously into the femoral artery
through an introducer sheath using the modified Seldinger technique.
Alternative routes of access include subclavian, axillary, brachial, or iliac
arteries. The catheter can also be inserted surgically using a
transthoracic or translumbar approach, but this is associated with an
increased periprocedural mortality.
Once vascular access is obtained, the balloon catheter is inserted and
advanced, usually under fluoroscopic guidance, into the descending
thoracic aorta, with its tip 2 to 3 cm distal to the origin of the left
subclavian artery (at the level of the carina)
The console is programmed to identify a trigger for balloon inflation and
deflation. 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.
The balloon is set to inflate after the aortic valve closure (which
corresponds to the dicrotic notch on the arterial waveform) and deflate
immediately before the opening of the aortic valve (which corresponds to
the point just before the upstroke on the arterial pressure waveform).
804
 IABP timing refers to inflation and deflation of the IAB in relation to the
cardiac cycle. The cardiac cycle is monitored by continuous display of the
arterial pressure waveform. As the balloon inflates at the onset of
diastole, a sharp and deep V is observed at the dicrotic notch.
Balloon inflation causes augmentation of diastolic pressure and a second
peak is observed. This peak is referred to as diastolic augmentation.
Diastolic augmentation is ideally higher than the patients systolic
pressure except when reduced stroke volume causes a relative decrease
in augmentation.
Depending upon the patients haemodynamic status, the balloon is
programmed to assist every beat (1:1) or less often (1:2, 1:4, or 1:8). With
haemodynamic improvement, the device can be weaned to less frequent
cycling before complete removal.
The device should never be left unused in situ to prevent thrombosis
Suboptimal timing of inflation and deflation of the balloon will result in
haemodynamic instability
Early inflation: inflation of the IAB before aortic valve closure
Late inflation: inflation of the IAB markedly after closure of the aortic
valve
Early deflation: premature deflation of the IAB during the diastolic phase
Late deflation: deflation of the IAB after the onset of systole

805
COMPLICATIONS
Transient loss of peripheral pulse
Limb ischaemia
Occlusion of a large aortic branch including renal, SMA, or subclavian
arteries with distal ischemia.
Acute aortic dissection or perforation.
Wound infection
Hemolysis, thrombocytopenia.
Thromboembolism
Compartment syndrome
Local vascular injuryfalse aneurysm, haematoma, bleeding from the
wound
Balloon rupture (can cause gas embolus)
806
 Balloon entrapment
Haematological changes, for example thrombocytopenia, haemolysis
Malpositioning causing cerebral or renal compromise
Cardiac tamponade
Patient care should be carried out with three primary goals in mind
Evaluation in terms of haemodynamic status, systemic perfusion, and
relief of cardiac symptoms;
Observation for early signs of complications including limb ischaemia,
balloon malpositioning, thrombus formation, bleeding, and infection;
Ensuring proper functioning of IABP, including correct timing, consistent
triggering, and troubleshooting of alarms.

807