PRE AND POST OPERATIVE

CARE FOR PATIENT AFTER

CARDIAC SURGERY

Submitted by Submitted to
Mrs. Gayathri R Mrs. Sasikala
2nd year MSc (N) Associate Professor
UCON Kollam UCON Kollam
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 Introduction
Cardiac surgery, or cardiovascular surgery, is surgery on the heart or great
vessels performed by cardiac surgeons. It is often used to treat complications of ischemic heart
disease (for example, with coronary artery bypass grafting); to correct congenital heart disease;
or to treat valvular heart disease from various causes, including endocarditis, rheumatic heart
disease, and atherosclerosis. It also includes heart transplantation.

Type of cardiac surgery

 Open heart surgery
 Modern beating heart surgery
 Heart transplant
 Coronary artery bypass grafting
 Minimally invasive procedure

Pre-operative care
Preoperative care refers to health care provided before a surgical operation. The aim
of preoperative care is to do whatever is right to increase the success of the surgery. At some
point before the operation the health care provider will assess the fitness of the person to have
surgery.
1. ADMISSION OF PATIENTS AND PREOPERATIVE WORK-UP
Investigations:
i. Chest X-ray - at least a new PA film. Most patients will have fairly recent films including a
penetrated PA to show cardiac chamber size. These films need not be repeated. A lateral film
is essential in anyone who has had a previous bypass operation to show the amount of space
behind the sternum and the number of wires. For coronary artery cases a PA film is sufficient.
ii.ECG.
iii. Respiratory Function Tests - FEV1, Vital Capacity, PEFR. If these tests are poor, arterial
blood gases breathing air are a useful baseline for postoperative care.
iv. Blood tests: Full Blood Count, Urea, Electrolytes, Liver Function Tests, Glucose,
Creatinine, Coagulation Studies, Hepatitis B & C Screening, Cross Matching (Usually 2- 6
Units). If significant chest disease ABG’s. v.
Doppler ultrasound of carotids (if previous history of stroke, TIAs or carotid bruits or age over
65 years) vi. Bacteriology: Nose and throat swabs for St. Aureus,
MSU, sputum if appropriate. (Performed by nursing staff.)
All patients are given Bactroban to use at home and once admitted pre operatively.
vii. Chest physiotherapy before operation in patients with known chest disease, eg. Chronic
airways disease. Sputum culture is particularly important in this group.
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 viii. Old notes, including cardiac catheter data are essential and should be obtained. (If the
cardiac catheter is more than 12 - 18 months old then may require repeating, particularly if the
previous disease was single or two vessel)
ix. Transthoracic Echocardiography (TTE): Left Ventricular assessment and Valves
assessment.
x. Consent for operation. (Including documentation of the major risks.)
xi. Height (cm) and weight (kg) to calculate surface area and body mass index.

2) PREOPERATIVE MODIFICATION OF TREATMENT

i) Anticoagulants - These are tailed off over a few days prior to operation. Patients should have
a coagulation screen measured on the preoperative day to confirm a virtually normal clotting
status on the day of operation. If the coagulation has not normalized then consider the use of
FFP. Vit K is very rarely used (If the operation is postponed then anticoagulants
should be temporarily restarted - this is particularly important with a history of previous
strokes).
ii) Aspirin and Clopidogrel- This has a significant effect in diminishing platelet function and
can lead to increased postoperative blood loss. Ideally it should be stopped 7-10 days before
surgery, if not, should be stopped on the day of admission of the patient - unless there is
unstable angina.
iii) Digoxin - Continued until the day before operation.
iv) Diuretics and Potassium Supplements - Continued until the day before operation.
v) Beta Blockers, Calcium Antagonists, Long Acting Nitrates - Patients with coronary artery
disease will frequently be taking a combination of these drugs. It is important not to interfere
with these drugs in any way but to continue them until the day before operation.
vi) Antihypertensives - Maintain until operation.
vii) Monoamine Oxidase Inhibitors - Must be discontinued at least three weeks preoperatively.
viii) Anti-diabetic Agents and Steroids - Should be noted and the appropriate perioperative
management will be decided by the Anesthetist and appropriate physician. Discuss with the
anesthetist whether sliding scale insulin is required.

3. ARRANGEMENTS FOR OPERATION

The definitive operating list must be submitted to the Theatre the day before surgery. In the
event of changes to the operating list it is important that Blood Bank should be informed as
early as possible.
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In the event of an emergency operation out of hours, all key groups must be informed. These
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are:
 i. Theatre.
ii. Consultant Anesthetist and Duty Anesthetic SR
iii. Perfusion Technician.
iv. Blood Bank.
v. CITU Staff. To confirm the availability of a bed on CITU for the postoperative care
of the patient.
vi. Involvement in all these tasks makes it easy to forget the patient and the anxious
relatives. Clearly they must be kept informed of plans and prospects.

4. OPERATING THEATRE
i. The SHO on theatre duty must be present at the scheduled starting time for anesthesia (usually
8.30 am), prior to theatre the theatre SHO’s should attend the ITU/HDU ward round.
ii. Male patient should be catheterized by the SHO but the anesthetic / theatre nurse will
catheterize female patients unless an emergency or no female staff are available.
iii. Current X-rays and hard copies of the Angiogram if available should be put on the viewing
box.
iv. Ensure that patient has been shaved properly. If not, shavers are available in the anaesthetic
room to remove additional hair.
v. Patients having re do surgery require external defibrillation pads to be attached to the chest
wall and the SHO must connect them once in theatre to the defibrillator
vi. Prophylactic antibiotics are given in the anaesthetic room by anesthetist 40-60 minutes
before knife to skin.

Alterations to antibiotics may be required for example, in patients undergoing surgery for
endocarditis. These will have been discussed preoperatively with Bacteriology and appropriate
therapy chosen.

Current Antibiotic Prophylaxis Regime

All patients (unless beta-lactam allergic) should receive:
• Cefuroxime 1.5 g @ induction
• 750 mg 8 hourly for 48 hours

High Risk patients should also receive in addition to Cefuroxime:

• Teicoplanin 800 mg @ induction
• Then three further doses of 800 mg 12 hrly
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 High risk category includes any of the following:
• “Pool” patients or patients from another hospital unless recent negative MRSA screen (< one
week)
• Patients received from any critical area
• Patients with no MRSA screen result available
• Emergencies
• Redo operations
• Obese patients (BMI > 30)
• Diabetic patients
• Intra cardiac procedures (Valve repair / replacements)
• Bilateral internal mammary artery grafts

Cefuroxime (beta-lactam) allergic patients should receive:

• Teicoplanin 800 mg and Ciprofloxacin 400 mg @ induction
• Then three further doses of Teicoplanin 800 mg and Ciprofloxacin 400 mg12 hrly
All antibiotic dosages and times should be clearly recorded on the patient’s drug chart
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  Post-operative care
Postoperative care is the care you receive after a surgical procedure. The type
of postoperative care you need depends on the type of surgery you have, as well as your
health history. It often includes pain management and wound care. Postoperative care begins
immediately after surgery.

Immediate post-op care

The resident should be present in the ICU when the patient arrives from the operating room
to receive a sign-over from the anaesthesiologist and the cardiac surgical team. During this
period, the ICU nurses will be transferring the patient to the ICU monitors and checking all
lines and infusions. The nurse will then do the initial set of hemodynamic readings. The
Respiratory Technician will place the patient on a ventilator. Unless the patient is unstable
it is best to stay out of the way of the nurses during this period, and wait until they are
finished with their assessment before examining the patient.

History
Collect the following information from the anaesthesiologist, surgeon, and the patient chart.

 Patient background (age, sex)

 Type of operation (CABG, valve, elective vs. urgent etc.)

 Indications for operation

 Pre-operative cath report (vessels involved, LVEF)

 Success of operation (completely or incompletely revascularized, difficulties,

complications)

 CPB time and aortic cross-clamp time

 Ease of separation from CPB ( dysrhythmias, need for inotropes, pacing, etc). Difficulty
coming off pump may imply problems with myocardial preservation or with the
revascularization.

 Current inotropes, vasopressors, or anti-hypertensive (if any)

 Need for cardiac pacing

 Use of Intra-aortic balloon pump (IABP), ventricular assist devices (VAD), or nitric
oxide (NO).
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 Significant bleeding
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  Other significant co morbidity, with emphasis on those conditions that may alter the
post-operative management or course (carotid artery disease, COPD, asthma, diabetes,
renal failure, hepatic failure, etc.)

 Pre-operative medications

 Allergies

Physical examination and assessment

 Assure that the endotracheal tube is in proper position and the patient has equal air entry
bilaterally. Remember that tube displacement or pneumothoraxes can occur or become
apparent at any moment.

 Verify that the patient's oxygen saturation is adequate. Check the ABG results as soon
as they are available.

 Verify correct ventilator settings.

 Check the initial hemodynamic readings (HR, BP, cardiac output and index, CVP,
PCWP) and determine what vasoactive infusions the patient is on and at what rates.

 Check the patient's heart rhythm. Verify pacemaker settings if the patient is connected
to one.

 Check the chest and mediastinal drainage sumps to ensure they are patent and that the
patient is not bleeding excessively.

 Examine heart sounds. Listen for murmurs particularly if the patient has had valve
surgery.

 Check all peripheral pulses. Do repeated assessments if there is concern for acute limb
ischemia or if the patient has a femoral arterial line or IABP in place.

 Examine the abdomen.

 Check pupillary reflexes. Do a more complete neurologic exam when the patient begins
to awaken from GA.
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 Labs and tests
Electrocardiogram

 changed from pre-op ( new RBBB is not uncommon, usually temporary and of little
clinical significance; Shifts of the axis are also common and usually benign)

 Rhythm - post-operative bradycardias, blocks, or atrial fibrillation

 ST-T changes - diffuse non-specific changes are not uncommon and may reflect
pericardial inflammation; ST elevation in two or more contiguous leads in a territory
that was grafted can indicate an acute graft failure - notify the ICU fellow or Attending
immediately; ST segment elevation across the anterior leads can represent LIMA spasm
if the LIMA was grafted to the LAD - notify the ICU fellow or Attending immediately.
Chest X-Ray

 Verify correct position of the ETT. Ideally half way between the glottis and the carina.
Should be at least one cm above the carina.

 Verify correct position of the Swan-Ganz catheter. The tip should not be too peripheral
- no more than 1 to 2 fingerbreadths beyond the lateral mediastinal shadow.

 Check the position of all other tubes and drains. The ng tube, chest tubes, and mediastinal
sumps.

 Check for pneumothorax.

 Check for lobar collapse, atelectasis, effusions, and pulmonary edema.

Laboratory Results

 Haemoglobin

 Coagulation parameters (PLT, PT, PTT, INR, ACT)

 Potassium, magnesium - a vigorous diuresis is common in the first few hours after the
OR. This can lead to significant hypokalaemia and hypomagnesaemia which increases
the likelihood of post-operative dysrhythmias. Standing orders are in place to replace
these electrolytes.

 Glucose - tight glycaemic control post-operatively reduces morbidity. Use an insulin

drip or sliding scale to keep the blood glucose between 6 and 10mMol/L.

 Cardiac markers - elevations of CPK, CPK-MB, and troponins are non-specific. They
should be assessed as part of the overall clinical picture including the hemodynamic
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status of the patient and the EKG.

 Warming

CPB is usually accompanied by hypothermia to < 32 C. Patients are usually warmed to at

least 34 C before transfer to the ICU.

Effects of hypothermia

 Predisposes to ventricular dysrhythmias and lowers VF threshold

 Increases SVR; increases afterload and myocardial workload

 Patient shivering causes increased peripheral O2 consumption

 Decreases CO2 production; a patient who has a respiratory alkalosis (low PCO2) on
initial ABG usually will increase their PCO2 with rewarming

 Coagulopathy; impairs platelet function and the coagulation cascade. Rewarming is an

important part of the treatment of a bleeding patient.
Patients are rewarmed using the "Bear Hugger". This blows warm air over the body surface
to warm by convection.

Bleeding
Bleeding can be divided into:

1. "Medical" bleeding secondary to defects in the coagulation cascade, platelets, or

fibrinogen;

2. "Surgical" bleeding secondary to operative trauma including leaks at sites of vascular

anastomosis or cannulation sites or bleeding from small mediastinal arteries or veins.
Surgical bleeding requires a return to the OR for re-exploration and haemostasis.
Surgical bleeding

Consider a "surgical" source of bleeding in the following situations:

1. Persistent bleeding in the absence of a specific haemostatic defect (normal coagulation

parameters)

2. Sudden onset of fresh, rapid bleeding; especially if associated with a preceding sudden
increase in BP. Note that repositioning the patient (turning on their side) may also cause
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the drainage of a pre-existing collection of "old" darker blood that had pooled in the
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thorax.
 3. Greater than 500 cc of bleeding in the first post-op hour.

4. > 400 cc/hr. x 2 hours.

5. > 300 cc/hr. x 3 hours

6. > 200 cc/hr. x 4 hours

If any of the above criteria are noted you must notify the ICU Fellow or Attending and the
Cardiac Surgery Fellow immediately. The ICU Fellow or Attending should be notified about
any significant bleeding whether it is believed to be "medical" or "surgical."

Etiology of "medical" bleeding:

1. Residual heparin effect; patients are anticoagulated before going on CPB with a large
dose of heparin to maintain their ACT >400. The heparin is 'reversed' at the end of the
case with protamine. Occasionally, the calculated dose of protamine given is not
sufficient to completely reverse the heparin effect. Patients may also receive additional
heparin if they are given back blood that remained in the bypass circuit when the patient
was disconnected from CPB ("pump blood"). A "heparin rebound phenomenon" can also
occur several hours post-op. An ACT will be done as soon as the patient arrives in the
ICU. Normal values are between 100 and 120 seconds.

2. Qualitative platelet defects. Platelet function may be impaired for several reasons. Many
patients are on anti-platelet agents pre-operatively. CPB also leads to impaired platelet
function, and the longer the duration of CPB, the greater the impairment.

3. Quantitative platelet defects. Platelet numbers can be decreased following CPB due to
hemodilution, destruction, and aggregation.

4. Clotting factor deficits. Hemodilution on CPB or consumption. Pre-operative defects

secondary to hepatic disease.

5. Fibrinogenolysis; plasminogen activation during CPB. Clinical DIC is rare.

Treatment of "Medical" Bleeding

1. Correct hypothermia.

2. Control BP if elevated.

3. Protamine 25 - 50 mg iv if ACT elevated. Note that an idiopathic "protamine reaction”

(i.e., pulmonary hypertension, hypoxia, and systemic hypotension) can occur with any
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dose, even if previous doses of protamine were well tolerated. In excessive quantities
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protamine is itself an anticoagulant.

 4. DDAVP 20 mcg iv. This has been shown to improve platelet function and decrease active
bleeding in uraemia or vonWillebrand's disease. It is given post-cardiac surgery because
it is felt it might improve platelet function although the data are mixed in this setting.

5. Platelet transfusion; usually 5 units for bleeding in the face of suspected or confirmed
defects in platelet function or number. Five units of platelets should raise the platelet
count by 25,000 to 50,000 and will also provide clotting factors equivalent t o 1 unit of
FFP. In a patient who is bleeding significantly, the goal is to keep the platelet count
greater than 100,000 of functional platelets.

6. Fresh Frozen Plasma - normally 2 to 6 units with each unit 200 to 250 ml. giving a total
of 20 cc/kg will replace factor levels to at least 50% of normal if you are starting at levels
of 0. In a bleeding patient the goal is to return the PT and PTT close to normal values.

7. Cryoprecipitate; contains fibrinogen and factor VIII. 1 unit is 20 to 25cc. usually given
pooled as 8 to 10 units for suspected or confirmed hypofibrinogenemia.

8. Antifibrinolytic agents; Episilon-aminocaproic acid (AMICAR), tranexemic acid, or

aprotinin. Inhibit conversion of plasminogen to plasmin thus preventing activation of
fibrinolysis. Ideally should confirm fibrinolysis before use (elevated D-dimers, low
fibrinogen). Risk of thrombosis including acute graft thrombosis, DVT, PE.

9. Raising the head of the bed or increasing the level of PEEP on the ventilator are also
used on occasion. The proposed mechanism of action for these therapies are to decrease
mediastinal venous pressure or increase pleural and mediastinal pressure thus stopping
small venous bleeding. Definitive studies are lacking.

10. PRBC; it is of utmost importance to maintain a haemoglobin level high enough to

maintain adequate oxygen delivery during the period of significant bleeding.
Ideally, the choice of therapy should be guided by haematological laboratory tests including
a CBC, PT, PTT, ACT, fibrinogen, and d-dimers. Practically speaking, one does not always
have the luxury of time with patients bleeding significantly and one may have to resort to
empiric or "shotgun" therapy.

Transfusion of Packed RBC's

The principle objective when giving PRBC's is the improvement of inadequate oxygen
delivery and the minimization of adverse outcomes as a result of this. In a patient who is
actively bleeding and thus who's haemoglobin mass is not in a steady state, one must be
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more liberal in transfusing PRBC's to avoid severe impairments in peripheral oxygen

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 delivery. However, with a patient who is not bleeding rapidly, one can take a more deliberate
approach to transfusion.

Remember that there are several potential risks associated with the transfusion of red blood
cells, including

1. Transfusion reactions (haemolytic, non-haemolytic, febrile)

2. Infections (hepatitis B, C, etc.; CMV, bacterial, parasitic)

3. Immunosuppression (increased sepsis)

The use of a single Hgb trigger for all patients, and other approaches that fail to consider all
important physiologic and surgical factors affecting oxygenation are not recommended. The
risk of complications from inadequate O2 delivery should determine the need for
transfusion. Signs of inadequate oxygen delivery include a low mixed venous oxygen
saturation, high lactic acid level, or clinical signs of organ dysfunction that cannot be
attributed to other causes. Most post-operative cardiac patients, who are hemodynamically
stable, are not actively bleeding, and are following an otherwise uncomplicated post-
operative course, tolerate an Hgb as low as 7.0 g/dL without problems.

Hemodynamic management
Hypotension and low cardiac output

1. BP = CO x SVR

2. CO = HR x SV (stroke volume)

3. Stroke volume is determined by preload, contractility, and afterload

4. Bradycardias or tachydysrhythmias that decrease ventricular filling can decrease C.O.

There are numerous causes for hypotension post-operatively. Proper management of the
hypotensive patient in the ICU requires that the precise etiology for the hypotension is
determined and therapy is directed towards reversal of this specific problem. Equation 1
demonstrates that hypotension can be caused by a "pump problem" (low cardiac output) or
a low SVR (arterial "circuit" problem). The following is an approach to managing the
hypotensive patient;

1. Look at the recent hemodynamic parameters.

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2. Assess the cardiac output/index. Is this a "pump" problem? Or is it due to low SVR?
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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;

 SIRS - a proportion of patients post CPB will have significant cytokine increases

 Sepsis

 Anaphylactic or anaphylactic reactions including protamine reactions,

 Drug-induced, toxicological - nitrates, antihypertensive, narcotics and sedatives, etc.

 Adrenal insufficiency (Was the patient steroid dependent pre-operatively?)

 Hyperthyroidism, hypothyroidism,

 Neurogenic (spinal) shock

 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 tachycardia’s

(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. Although the CVP in normal
individuals varies between 0 and 4 mmHg, patients immediately post-op cardiac surgery
commonly have decreased cardiac compliance for multiple reasons. In fact the majority
of uncomplicated patients have CVP's in the 6 to 10 mmHg range. Remember, what you
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really are interested in is a volume measurement (preload= right or left end-diastolic

volume), but what you are measuring are pressures (CVP or PCWP = Right or left
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 ventricular end-diastolic pressures). Therefore if the compliance worsens (ventricle
"stiffens") the same or even a lesser volume can give a higher pressure. If you think the
patient may be "preload responsive" (i.e., on the ascending portion of Starling's curve so
that an increase in preload will increase cardiac output), then give the patient a fluid
bolus. The amount is usually between 250 and 500 cc but should be at least enough to
raise the CVP by 3 to 4 mmHg. Both crystalloids (normal saline) and colloids
(Pentaspan) can be given. Although there may be theoretical reasons to choose one over
the other, there is no convincing clinical evidence that one is superior. If the CVP
increased by 3-4 but the cardiac output did not increase, then the patient is on the flat
portion of the Starling curve and is not pre-load responsive. The absence of respiratory
variation on the CVP monitor tracing is also suggestive that the patient has an adequate
preload and that further volume therapy is unlikely to increase cardiac output. Remember
that PEEP can decrease preload by decreasing venous return.

 High afterload. Secondary to vasoconstriction and hypertension.

 Decreased contractility. This should be managed with inotropic agents while

simultaneously looking for the cause.

 Low pre-operative ejection fraction

 Prolonged CPB time or cross-clamp times, difficulty with myocardial protection

intra-op

 Acute bypass graft occlusion (check the ECG)

 Graft spasm (especially LIMA) - check the ECG for ST elevation

 Tamponade .

 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.
Inotropes and vasopressors

The following is a very simplified approach to the choice of inotropes and vasopressors.
More information can be found at the Critical Care Drug Manual - London Health Sciences
Centre, UWO.

Inotropes
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1. Adrenergic (catecholamine)
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  Dobutamine - beta-agonist (ß1 >ß2). Increases contractility and HR. ß2 effect can
sometimes decrease SVR and BP. ß1 effect can cause dysrhythmias. Start at 2.5
mcg/kg/min. Titrate upward by 2.5 mcg/kg/min until adequate cardiac index.
Maximum 15 to 20 mcg/kg/min. Notify ICU Fellow or Attending if at 10 mcg/kg/min
or higher.

 Epinephrine -alpha and beta agonist (ß > alpha). Increases HR, CO, and SVR.
Generally a second-line inotrope. A subset of patients who do not respond to
dobutamine will respond to epinephrine. Potential detrimental effects include
significant increases in myocardial oxygen consumption, increased lactic acidosis,
arrhythmias. Start at 0.5 to 1.0 mcg/min and increase by these amounts until adequate
cardiac index. Notify ICU Fellow or Attending if > 5 mcg/min and each increase of
5 mcg/min above that.

 Dopamine - stimulates dopaminergic, beta, and alpha receptors in dose-dependent

fashion. Inotropic effect (beta-effect) predominates in the 5 to 10 mcg/kg/min range.
Notify ICU Fellow or Attending if at 10 mcg/kg/min or higher. There appears to be
little benefit over Dobutamine as an inotrope. In low doses (2 - 4 mcg/kg/min) it has
been purported to have beneficial renal protective effects ("renal-dose dopamine").
While it can increase urine output by several mechanisms, there is little evidence that
it improves creatinine clearance or decreases the incidence of acute renal failure.

2. Phosphodiesterase inhibitors

 Milrinone - phosphodiesterase inhibitors decrease the metabolism (breakdown) of

cAMP. cAMP is the "second messenger" that leads to increased calcium availability
at the actin-myosin complexes and thus increased contractility. Beta-receptor
stimulation leads to increases in cAMP. Thus the use of phosphodiesterase inhibitors
"bypass" the beta-receptor. Milrinone increases cardiac output. It also decreases
Pulmonary Vascular Resistance (PVR) and thus can be useful if pulmonary
hypertension or significant right ventricular dysfunction is a problem. The bolus dose
is 50 mcg/kg followed by an infusion between 0.375 and 0.75 mcg/kg/min. The half-
life of milrinone is several hours, unlike the catecholamine’s that have half-lives of
a few minutes. When weaning milrinone, the rate of decreases should be slower and
more gradual than with dobutamine or epinephrine. Reassess the patient 4 to 6 hours
later to verify that he or she has tolerated the decrease.
Vasopressors
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1. Adrenergic (catecholamine)
  Norepinephrine (Levophed) -Strong alpha agonist with beta activity as well. Causes
vasoconstriction and thus increases SVR and BP. Theoretically, since it has inotropic
activity as well, it is less likely to cause a decrease in cardiac output due to increased
afterload compared to a pure alpha agonist such as phenylephrine. Negative effects
include myocardial and mesenteric ischemia, LIMA spasm, dysrhythmias, and
decreased cardiac output due to afterload increases. Starting dose is usually 2 to 5
mcg/min. Notify the ICU Attending or Fellow if the dose is increased to 10 mcg/min
and each additional increase of 5 to 10 mcg/minute beyond that.

 Phenylephrine (Neosynephrine) - Pure alpha agonist. Can be used as a continuous

infusion but more commonly used as bolus infusions of 100 to 200 mcg for sudden
severe hypotension not responding to volume infusion.

2. Peptides

 Vasopressin - used for hypotension with a normal or high cardiac output and low
SVR state that is refractory to norepinephrine. Has a significant side effect profile
including myocardial and mesenteric ischemia. Should only be used after discussion
with the ICU Attending.

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 specifi c
enough to absolutely rule in or out tamponade.

A "typical" presentation would be a patient who had a normal ejection fraction pre -
operatively, underwent uncomplicated ACBG, initially had excellent hemodynamic
parameters, bled from the mediastinal sumps moderately, then the bleeding "stopped" or
blood ceased to drain from the sumps. (Always check to make sure the sumps 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.
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1. Search for alternate explanations for the low cardiac output (i.e., hypovolemia,
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myocardial ischemia, etc.).

 2. Assure patency of the sumps.

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 results in an elevation and equalization of the CVP, PCWP,
and PAD associated with low CO. (CVP=PCWP=PAD). 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.

4. Look for a "loss of the y-descent" on the CVP or PCWP tracing. Remember that the "y-
descent" occurs at the beginning of diastole when the AV valves open. In the usual
situation, there is a pressure gradient between the atrium and the ventricle because the
ventricle has just emptied and the atrium has filled while the AV valve was closed during
systole. Thus, there is a rapid transfer of blood from atrium to ventricle and the pressure
drops significantly in the atrium - the "y-descent". In tamponade, the external pressure
on the ventricle decreases the pressure gradient between the atrium and the ventricle.
The atrium does not empty into the ventricle rapidly because ventricular filling is
impeded. Thus the "y-descent" is minimal or absent.

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-oesophageal
Echo (TEE) will be required because of poor "windows" common in the post-operative
state with Trans-thoracic echo (TTE). The Echo cardiographer on call should be paged
after discussion with the ICU Fellow or Attending.

7. The only treatment for cardiac tamponade is return to the OR, re-sternotomy, and
evacuation of the clot with haemostasis of any ongoing bleeding. The cardiac surgery
fellow should be notified early if potential tamponade is suspected. 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) an urgent sternotomy should be done in the ICU. This should only be
done by the Cardiac Surgeon or Cardiac Surgery Fellow. Page them STAT and move
the thoracotomy tray to the bedside while following standard ACLS algorithms.
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 Mechanical assist devices
Intra-aortic balloon pump

The IABP consists of a long cylindrical balloon placed at the end of a catheter placed in the
descending thoracic aorta. The tip of the catheter should be positioned just distal to the left
subclavian artery. The balloon should also be placed so that it does not occlude the renal or
mesenteric arteries. Helium is pumped into the balloon to inflate it at the beginning of
diastole. The balloon is deflated at the end of diastole. It has been described as the "ideal
inotrope". In the failing heart it can decrease myocardial workload while increasing coronary
perfusion.

1. "Augmentation." By inflating at the beginning of diastole (just after the closure of the
aortic valve), the aortic diastolic pressure is increased or "augmented", thus improving
coronary perfusion. Remember, left ventricular coronary flow occurs during diastole
with the gradient to flow being the difference between the aortic diastolic pressure
(ADP) and the right atrial pressure (RAP). That is CPP = ADP - RAP.

2. "Diastolic decrement" .The balloon deflates just before cardiac systole (just before
opening of the aortic valve). This leads to a sudden decrease in the aortic pressure and
thus LV afterload.

3. The IABP can be adjusted so that the balloon inflates and deflates with every cardiac
cycle (1:1), every second cardiac cycle (1:2), or every third cardiac cycle (1:3). It is also
possible to decrease the volume the balloon inflates to by decreasing the amount of gas
injected into it.

4. "Timing". Two methods are commonly used to time or "trigger" the IABP. It can be
triggered from the arterial waveform recorded from the catheter tip, or it can be timed to
the QRS complex of the cardiac monitor. The arterial waveform usually works better if
the patient is having arrhythmias. The IABP should inflate just after closure of the aortic
valve. This corresponds to the dicrotic notch on the arterial waveform. If it inflates too
late, its ability to "augment" and effectiveness will be limited. It should deflate just
before left ventricular ejection. If it remains inflated during early systole it will impair
LV ejection. If it deflates too early in diastole its ability to afterload reduce will be
limited. The IABP console allows for manual adjustment of the balloon inflation and
deflation. A cardiac perfusionist is always on call to help with adjustment of balloon
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timing or any "trouble-shooting" that may be required.

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 Indications

1. Post-operative cardiogenic shock not responding to medical therapy.

2. Acute myocardial ischemia including medically-refractory ischemia pre-operatively and

post-operative myocardial ischemia.

3. Acute mitral regurgitation or ventricular septal rupture.

4. Bridge to cardiac transplantation.

Contraindications

1. Aortic insufficiency

2. Aortic dissection

3. severe peripheral vascular disease

Complications

1. Leg ischemia. The most common complication. Distal pulses should be monitored at
least hourly.

2. Occlusion of a large aortic branch including renal, SMA, or subclavian arteries with
distal ischemia.

3. Acute aortic dissection or perforation.

4. Hematoma at insertion site.

5. Wound infection

6. Hemolysis, thrombocytopenia, Thromboembolism

Conclusion
The most common surgical procedure encountered is the Aorto-Coronary Bypass Graft
(ACBG) for various indications such as left main coronary artery stenosis, severe triple-
vessel disease, angina refractory to medical therapy, or recurrent CHF due to ischemia.
Other surgical procedures, concomitantly with ACBG or alone, include valve repair or
replacements, repair of congenital or acquired defects (ASD, VSD, etc.), and repair or
replacement of the aortic root. Less common are removal of intracardiac tumours and LV
aneurysmectomy.
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To perform the surgery, the patient is usually put on "pump" or cardiopulmonary bypass
Page

(CPB). This involves cannulation of the right atrium and aorta (and later cross-clamping of
 the aorta), allowing the entire cardiac output to bypass the patient's heart and lungs. Blood
flow is maintained using a pump and the blood is oxygenated via a membrane oxygenator
incorporated into the circuit. Several myocardial preservation techniques are used to protect
the heart from ischemic damage during this period. Cardiologic arrest is induced using a
hyperkalemic solution to induce asystole and thus decrease myocardial metabolism and
oxygen consumption. The heart is usually cooled. The patient is also usually systemically
cooled to < 32 C to minimize peripheral oxygen consumption.

Bibliography
 Wongs;Merilyn,Essentials of Pediatric Nursing,8th edition,Elsievier Publication.
 Rimple Sharma, Essentials of Pediatric Nursing, 2th edition, Jaypee Brothers Medical
Publishers.
 Manoj Yadav, A Text Book of ChildhealthNursing, 2011 edition, Choice books &
printers (P) ltd.
 https://www.mcgill.ca/criticalcare/teaching/protocols/cardiac
 https://journals.lww.com/nursing/Fulltext/2004/07000/Caringfor_a_patient_after_CA
BG_surgery
 http://www.cardiothoracicsurgeryservices.com
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