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surgery patients
Introduction to cardiac surgery
History
Warming
Bleeding
Surgical bleeding
Hemodynamic management
Tamponade
While "on pump", the patient's BP and cardiac output are controlled by by the perfusionist
and also the anesthesiologist by means of vasoactive medications and inotropes. During this
time, the patient must by systemically anticoagulated with heparin to an ACT >400 to
prevent clotting in the bypass circuit. Long pump times are associated with increased post -
operative complications such as bleeding, myocardial stunning, and multi-system organ
failure. CPB also seems to be associated with the induction of a systemic inflammatory
response syndrome (SIRS). It is sometimes difficult to liberate the patient from CPB or "get
him off pump." That is, to restart the heart contracting normally. Pressors or inotropes are
often used in order to aid "coming off pump." A variety of dysrhythmias also may occur
during this period including bradycardias requiring pacing. Most often, these dysrhythmias
are transient and resolve.
In the past few years, more cases are being done with "beating heart" or "off pump". The
advantages of Off-pump Coronary Artery Bypass (OPCAB) are that the patient is not exposed
to the possible deleterious effects of CPB.
In some operations involving the aortic root, cross-clamping and cannulation of the aorta are
not feasible. In these situations the technique of Deep Hypothermic Circulatory Arrest
(DHCA) may be used. The patient is systemically cooled as much as possible (usually below
28 C) and a large dose of barbiturates are given as a neuroprotective agent. The circulation is
then completely arrested for a brief period of time to allow completion of the surgical
anastomosis.
History
Collect the following information from the anesthesiologist, surgeon, and the patient chart.
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.
Use of Intra-aortic balloon pump (IABP), ventricular assist devices (VAD), or nitric oxide
(NO).
Significant bleeding
Other significant co morbidity, with emphasis on those conditions that may alter t he
post-operative management or course (carotid artery disease, COPD, asthma, diabetes,
renal failure, hepatic failure, etc.)
Pre-operative medications
Allergies
Verify that the patient's oxygen saturation is adequate. Check the ABG results as soon as
they are available.
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.
Check pupillary reflexes. Do a more complete neurologic exam when the patient begins to
awaken from GA.
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.
Laboratory Results
Hemoglobin
Potassium, magnesium - a vigorous diuresis is common in the first few hours after the
OR. This can lead to significant hypokalemia and hypomagnesaemia which increases the
likelihood of post-operative dysrhythmias. Standing orders are in place to replace these
electrolytes.
Glucose - tight glycemic 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
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
Decreases CO2 production; a patient who has a respiratory alkalosis (low PCO2) on
initial ABG usually will increase their PCO2 with rewarming
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:
Surgical bleeding
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
the drainage of a pre-existing collection of "old" darker blood that had pooled in the
thorax.
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."
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.
1. Correct hypothermia.
2. Control BP if elevated.
4. DDAVP 20 mcg iv. This has been shown to improve platelet function and decrease active
bleeding in uremia 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 to 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.
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 hemoglobin level high enough to
maintain adequate oxygen delivery during the period of significant bleeding.
Ideally, the choice of therapy should be guided by hematological 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.
The principle objective when giving PRBC's is the improvement of inadequate o xygen
delivery and the minimization of adverse outcomes as a result of this. In a patient who is
actively bleeding and thus who's hemoglobin mass is not in a steady state, one must be more
liberal in transfusing PRBC's to avoid severe impairments in peripheral oxygen 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
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 a 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)
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;
2. Assess the cardiac output/index. Is this a "pump" problem? Or is it due to low SVR?
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.
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
Hyperthyroidism, hypothyroidism,
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 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 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 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.
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.
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
1. Adrenergic (catecholamine)
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.
2. Phosphodiesterase inhibitors
Vasopressors
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 eff ects
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.
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 specific
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.
1. Search for alternate explanations for the low cardiac output (i.e., hypovolemia,
myocardial ischemia, etc.).
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). The Echocardiographer 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 hemostasis 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.
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 timing or any
"trouble-shooting" that may be required.
Indications
Contraindications
1. Aortic insufficiency
2. Aortic dissection
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.
5. Wound infection
6. Hemolysis, thrombocytopenia.
7. Thromboembolism
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