Introduction to cardiac surgery
Immediate post-op care
Introduction to cardiac surgery
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 tumors and LV aneurysmectomy.
To perform the surgery, the patient is usually put on "pump" or cardiopulmonary bypass (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. Cardioplegic 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.
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.
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 anesthesiologist 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.
Collect the following information from the anesthesiologist, 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-hypertensives (if any)
- Need for cardiac pacing
- 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 the post-operative management or course (carotid artery disease, COPD, asthma, diabetes, renal failure, hepatic failure, etc.)
- Pre-operative medications
Physical exam and assessment
- Assure that the endotracheal tube is in proper position and the patient has equal air entry bilaterally. Remember that tube displacement or pneumothoraces 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.
Labs and tests
- ? 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.
- 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, pulmonary edema.
- 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 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.
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 can be divided into:
- "Medical" bleeding secondary to defects in the coagulation cascade, platelets, or fibrinogen;
- "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 hemostasis.
Consider a "surgical" source of bleeding in the following situations:
- Persistent bleeding in the absence of a specific haemostatic defect (normal coagulation parameters)
- 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.
- Greater than 500 cc of bleeding in the first post-op hour.
- > 400 cc/hr x 2 hours.
- > 300 cc/hr x 3 hours
- > 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:
- 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.
- 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.
- Quantitative platelet defects. Platelet numbers can be decreased following CPB due to hemodilution, destruction, and aggregation.
- Clotting factor deficits. Hemodilution on CPB or consumption. Pre-operative defects secondary to hepatic disease.
- Fibrinogenolysis; plasminogen activation during CPB. Clinical DIC is rare.
Treatment of "Medical" Bleeding
- Correct hypothermia.
- Control BP if elevated.
- 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 dose, even if previous doses of protamine were well tolerated. In excessive quantities protamine is itself an anticoagulant.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
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 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
- Transfusion reactions (hemolytic, non-hemolytic, febrile)
- Infections (hepatitis B, C, etc.; CMV, bacterial, parasitic)
- 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 a Hgb as low as 7.0 g/dL without problems.
Hypotension and low cardiac output
- BP = CO x SVR
- CO = HR x SV (stroke volume)
- Stroke volume is determined by preload, contractility, and afterload
- 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;
- Look at the recent hemodynamic parameters.
- Assess the cardiac output/index. Is this a "pump" problem? Or is it due to low SVR?
- Look at the cardiac rhythm.
- Look at the CVP to assess preload.
- Is the afterload high ?
- Is contractility decreased ?
- 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
- Anaphylactic or anaphylactoid reactions including protamine reactions,
- Drug-induced, toxicological - nitrates, antihypertensives, 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 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. 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.
- 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.
- 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.
- 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.
- 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 catecholamines 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.
- 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.
- 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.
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.
- Search for alternate explanations for the low cardiac output (i.e., hypovolemia, myocardial ischemia, etc.).
- Assure patency of the sumps.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
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.
- "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.
- "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.
- 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.
- "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.
- Post-operative cardiogenic shock not responding to medical therapy.
- Acute myocardial ischemia including medically-refractory ischemia pre-operatively and post-operative myocardial ischemia.
- Acute mitral regurgitation or ventricular septal rupture.
- Bridge to cardiac transplantation.
- Aortic insufficiency
- Aortic dissection
- severe peripheral vascular disease
- Leg ischemia. The most common complication. Distal pulses should be monitored at least hourly.
- Occlusion of a large aortic branch including renal, SMA, or subclavian arteries with distal ischemia.
- Acute aortic dissection or perforation.
- Hematoma at insertion site.
- Wound infection
- Hemolysis, thrombocytopenia.
Further information on the IABP can be found at the following websites:
Intra-Aortic Balloon Pumping - Internet Journal of Thoracic and Cardiovascular Surgery
IABP - A systematic review of the literature
IABP - A practical teaching module
Pat Melanson, MD, FRCPC
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