Critical Care of the Cardiothoracic Surgery Patient
Potential postoperative complications in cardiothoracic surgery patients include:
Acute kidney injury (AKI)
1. Description of the problem
Arrhythmias: Up to one third of cardiothoracic surgery patients develop supraventricular tachycardias postoperatively. More malignant ventricular arrhythmias are much less frequent (approximately 2%), but are potentially fatal.
Bleeding: There are many factors that predispose patients to bleeding in the immediate postoperative period. It is important to identify the cause(s) of coagulopathy- particularly surgical bleeding- and treat the patient accordingly.
Acute Kidney Injury: AKI develops in 30-40% of cardiothoracic patients postoperatively. There is variability in the severity of renal dysfunction, but even a mild renal injury portends increased postoperative morbidity and mortality.
Low Cardiac Output: Ensuring maintanence of an adequate cardiac output is a cornerstone of management of the postoperative cardiothoracic surgery patient. Cardiac Index, which is expressed as liters per square meter, is the customary clinical measure of cardiac performance.
2. Emergency Management
Atrial and ventricular arrhythmias should be managed as per AHA/ACC Advanced Cardiac Life Support (ACLS) Guidelines.
Urgent cardioversion of any arrhythmia is indicated if it leads to:
-Shortness of breath
-Altered mental status
or in the presence of ventricular fibrillation or pulseless ventricular tachycardia.
Urgent re-exploration is indicated if:
-There is indication of cardiac tamponade
-The patient is hemodynamically unstable secondary to hypovolemia
Distinguish surgical bleeding from a postoperative coagulopathy.
Establish the rate of bleeding per 15 minutes.
Determine and monitor the hemodynamic status of the patient.
Acute Kidney Injury
Once renal dysfunction becomes evident, prompt and aggressive strategies are required to prevent irreversible dysfunction or the need for dialysis.
Cardiac function should be optimized; a higher target mean arterial pressure (80-100 mmHg) may be required in some chronically hypertensive patients.
Careful fluid challenges are given to increase preload, as required.
Inotropic support can be used to improve cardiac contractility.
All potentially nephrotoxic drugs (particularly ACEi/ARBs or NSAIDs) should be stopped.
Low Cardiac Output
Emergency treatment of low-cardiac-output states must involve consideration of potential underlying causes (see below).
Urgent transthoracic echocardiography can be used to confirm the presence of cardiac tamponade, which would require return to the OR.
Heart rate should be increased to 90-100 bpm. This can usually be done via the epicardial pacemaker.
If hypotensive (SBP <100 mmHg or MAP <70 mmHg) and low left atrial pressure (LAP) or pulmonary artery diastolic pressure <15 mmHg, give fluid bolus (crystalloid or colloid).
If hypotensive (SBP <100 mmHg or MAP <70 mmHg) and high LAP (or pulmonary artery diastolic pressure) > 15 mmHg, commence inotropic support (dobutamine, dopamine, etc.).
Blood should be given to ensure hemoglobin >8 gm/dl.
A new onset of a cardiac arrhythmia is usually readily diagnosed by a change in the observed telemetry tracings.
An ECG should be performed daily and can help to differentiate between more subtle rhythm changes (eg, sinus rhythm with frequent PACs vs atrial fibrillation).
Changes in the rhythm are often associated with acute decreases in blood pressure.
The output from the chest drain aids in the diagnosis of excessive bleeding.
Bleeding is excessive if it totals 500 mL/hr in the first hour, 400 mL/hr in the first 2 hours, 300 mL/hr in the first 3 hours or 200 mL/hr in the first 6 hours.
Sudden increases in bleeding rate may signify underlying bleeding from an arterial or cardiac source.
Routine postoperative laboratory tests should screen for an underlying coagulopathy.
Activated partial thromboplastin time (aPTT) – increased with excess heparin, fibrinolysis or excessive consumption (eg, DIC).
Platelet count/Platelet function tests – useful if thrombocytopenia or platelet dysfunction
Fibrinogen – is significantly decreased in DIC
Thromboelastogram – can give a rapid overview of clotting derangements.
A comparison of the blood hematocrit between a freshly drawn sample and one from the chest tube will differentiate lymphatic drainage or excessive serum reflux from fresh bleeding.
Acute Kidney Injury
The RIFLE and Acute Kidney Injury Network (AKIN) criteria have been established to define AKI within any setting and have been widely adopted within intensive care medicine.
RIFLE is an acronym for Risk (R), Injury (I), Failure (F), Loss (L) and End stage (E) based on increases in serum creatinine or oliguria.
R, I and F are defined as increases in serum creatinine of 50%, 100% or 200% or oliguria for 6, 12 or 24 hours, respectively.
Loss is defined as AKI persisting >4 weeks.
End stage is defined as >3 months.
The AKIN working group has defined AKI as a reduction in kidney function over a period of 48 hours.
This is manifest as an absolute increase in serum creatinine of 0.3 mg/dl (25 μmol/L), or a relative increase in creatinine of 50% or more.
A documented oliguria of <0.5 mL/Kg/hr for >6 hours despite adequate fluid resuscitation is also considered AKI.
The AKIN group advocates 3 stages of AKI based on the R, I and F categories of RIFLE, where stage 1 is defined using the same criteria as R, and stages 2 and 3 are I and F respectively.
There is also increasing evidence to support the use of novel urinary and serum biomarkers (such as neutrophil gelatinase-associated lipocalin kidney injury molecule-1, and cystatin C) to improve the early and accurate diagnosis of AKI in the setting of intensive care.
Though the evidence supporting the use of these markers is growing, they are not yet in widespread use.
Low Cardiac Output
A normal cardiac index (CI) after surgery is between 2 and 4.4 L/min/m2.
Through the Fick equation, cardiac output (CO) is calculated by: CO = O2 consumption (mL/min/m2) / arteriovenous O2 difference (mL/L)
Arteriovenous difference is calculated by (SaO2 – SvO2) x 1.39(Hb) x 10, where SaO2 is the arterial saturation and SvO2 is the venous saturation.
CI is calculated by dividing CO by body surface area.
In the absence of available CO measurements, the CI will usually be >2.5 L/min/m2 if MAP 70-80 mmHg, urine output > 1 ml/kg/hr, base deficit < 2, skin temperature 36.5 -37.5 degrees and there are palpable pedal pulses.
To further delineate the cause of the low cardiac output, the following investigations should be considered:
Chest x-ray can rule out the presence of a pneumothorax.
ECG to exclude any new ST-segment changes indicative of potential new coronary artery or conduit occlusion.
Complete blood count to assess any drops in Hb or hematocrit indicative of ongoing bleeding, as well as leukocyte count elevation from underlying sepsis.
Echocardiography (preferably transesophageal) is most useful and will aid in the diagnosis of cardiac tamponade, new valvular dysfunction, regional wall motion abnormalities suggesting underlying ischemia, as well as right ventricular dysfunction.
Labortatory investigations for bleeding:
Complete blood count
Coagulation profile including INR and aPTT
Activated clotting time (ACT) is usually done at in the ICU.
4. Specific Treatment
Arrhythmias should be managed as per AHA/ACC Advanced Cardiac Life Support (ACLS) guidelines.
Prophylactic use of beta-blockers has decreased the incidence of atrial fibrillation by 70-80%.
In postoperative patients with atrial fibrillation, ensure that electrolytes are replete and there is no underlying sepsis.
Beta-blockers are first line for ventricular rate control, and amiodarone can be used to attempt chemical cardioversion.
Vernakalant is a novel, relatively atrial selective, anti-arrhythmic drug that has shown efficacy in the cardioversion of atrial fibrillation to sinus rhythm in a post-CABG cohort.
First-line treatment for hemodynamically stable ventricular tachycardia is amiodarone.
Ensure patient is normothermic. Use a Bair Hugger blanket if necessary.
Reverse elevated activated clotting time (ACT) with protamine sulfate 25-100 mg, which is given slowly.
Stop any “pump blood” that is being administered.
Give platelets if count <100 x 109/L.
Give fresh frozen plasma if INR >1.3.
Give packed red blood cells if hemoglobin <8 g/dL.
Treat hypertension, which may be placing stress on the anastomotic lines.
Consider increasing the PEEP to 12 cm H2O to increase intrathoracic pressure.
For refractory bleeding, the patient should be returned to OR for re-exploration and definitive treatment of the bleeding.
Monitor the patient’s hemodynamic status every 15 minutes, or continuously as needed.
Acute Kidney Injury
The initial management of oliguria is to optimize blood volume and cardiac output, and eliminate the use of vasoconstrictors as tolerated.
In established renal failure, early and aggressive renal replacement therapy has been shown to decrease mortality.
Renal replacement therapy may be delivered continuously or intermittently, as tolerated hemodynamically while achieving desired control of fluid balance and azotemia/electrolytes.
Low Cardiac Output
Inotropic agents can be used to improve ventricular contractility.
The agents most commonly used are the catecholamines dobutamine, dopamine, epinephrine and norepinephrine.
Hemodynamic effects can be dose-dependent.
Dobutamine and dopamine enhance heart rate and contractility similarly.
Dobutamine will lead to a greater improvement in coronary blood flow as well as improved reduction in preload and afterload.
At low doses, epinephrine causes vasodilatation via β2 adrenergic receptors; at higher doses it causes vasoconstriction via α-adrenergic receptor stimulation.
Norepinephrine is used in situations of hypotension in good to normal CO (eg, sepsis).
Milrinone is a phosphodiesterase inhibitor that can be used synergistically with catecholamines.
It is a potent vasodilator and inotrope, and is particularly useful in the setting of pulmonary hypertension.
Intra-aortic balloon pumps (IABPs) can augment coronary perfusion, improve stroke volume, decrease afterload and increase CO.
Contraindications to the use of an IABP include severe atherosclerosis of the iliofemoral vessels, aortic dissection and aortic insufficiency.
The optimal timing of placement for IABPs remains controversial, including which high-risk group may benefit from prophylactic placement.
5. Disease monitoring, follow-up and disposition
Patients with persistent atrial fibrillation postoperatively should be started on anticoagulation to decrease the risk of CVA. Elective DC cardioversion can be carried out 6-8 weeks after discharge if the patient remains in atrial fibrillation at this time.
If bleeding is due to a coagulopathy, there should be a resolution of bleeding once the coagulopathy has been reversed. If the patient continues to bleed with a normal temperature and coagulation profile, the cause of the bleeding is likely to be surgical in nature.
Ensure chest drains do not clot off, giving the false impression of resolution of the bleeding.
If CO is not improving with the addition of inotropes, an urgent echocardiogram should be obtained and cardiology consultation should be considered.
The possible etiology of the reduced function should be defined (see pathophysiology section below).
Postoperative AKI leads to increased 30-day and 1-year mortality in patients post-CABG.
Follow-up with a nephrologist is advised for patients who have developed postoperative AKI, whether the serum creatinine returns to baseline postoperatively or not.
The mechanism for postoperative atrial fibrillation is not well understood, but it is thought to include multiple wavelet reentry in the atria, rapid firing of an atrial focus, or rarely atrial ischemia.
Ventricular tachycardia following CABG is often related to areas of scarring from underlying ischemia.
The scarring in the LV forms a substrate for reentry.
Patients with a history of larger infarcts and as a result poorer LV function are more likely to develop VT.
Medical bleeding may be due to:
–An elevated activated clotting time (ACT). This may be due to the administration of heparin during surgery or “pump blood” in the ICU.
–Preoperative treatment with platelet inhibitors such as aspirin, clopidogrel, and prasugrel
–Low platelet count, secondary to preoperative thrombocytopenia and hemodilution on bypass
–Low fibrinogen, secondary to hemodilution on bypass
–Fibrinolysis secondary to plasminogen activation on cardiopulmonary bypass
Surgical bleeding may be due to:
–Anastomotic suture line or cannulation sites
–The internal mammary artery bed and the pericardium
–Side branches of arterial or venous conduits
–The sternal periosteum or sternal wire holes
–Chest drain insertion damaging intercostal artery
Acute Kidney Injury
There are multiple hypothesized causes of cardiopulmonary bypass-associated oliguria and/or AKI, including:
Generation of reactive oxygen species
Activation of inflammatory pathways
These effects are related to the effects on renal physiology of the sustained period of hyopthermic, nonpulsatile low-flow renal perfusion associated with bypass, as well as the endocrine and CNS effects of major surgery.
Vasoconstriction occurs secondary to angiotensin II and an increase in catecholamines.
Activation of the renin-angiotensin-aldosterone system promotes sodium and water retention and potassium excretion
Complement, bradykinin and kallikrein are increased, increasing capillary permeability and causing a fluid shift into the interstitium.
Low Cardiac Output
The etiologies of low cardiac output can be subdivided into pre-, intra- and post-operative causes.
Preoperative – baseline ventricular dysfunction secondary to previous myocardial infarction or valvular heart disease, pulmonary hypertension
Intraoperative – poor myocardial protection, incomplete revascularization or repair of valvular lesions
Postoperative – decreased contractility due to myocardial stunning or ischemia secondary to conduit spasm or thrombosis, dysrhythmias, decreased LV preload (eg, hypovolemia), cardiac tamponade, tension pneumothorax, valve thrombosis or dehiscence, RV dysfunction secondary to pulmonary hypertension
Myocardial compliance and contractility fall postoperatively secondary to myocardial edema.
Ischemia-reperfusion injury also contributes to a decline in myocardial function for 6-8 hours after surgery, before it returns to baseline.
Due to factors such as bleeding, loss of arterial and venous tone and increased capillary permeability, volume replacement is frequently required after surgery to maintain adequate preload.
Atrial fibrillation is common after cardiothoracic surgery and can occur in up to 40% of patients post CABG or 65% of patients undergoing combined CABG and valve surgery.
Risk factors for developing AF include older age, male sex, prior AF, hypertension and congestive cardiac failure.
Up to 80% of patients who develop AF will revert to sinus rhythm within 24 hours.
The average blood loss during “on-pump” cardiothoracic surgery is 1 liter.
3-5% of patient have significant blood loss (>100 ml per hr for 2 hours). This percentage increases to approximately 19% with emergency cases post-thrombolysis.
Surgical re-exploration is required in approximately 2% of patients undergoing CABG.
AKI complicates 30-40% of pediatric and adult cardiothoracic surgeries.
AKI requiring dialysis occurs in 1.5% of patients.
Risks for developing AKI include age, diabetes, previous renal function, surgery type, preoperative IABP, LV ejection fraction <35% and chronic obstructive lung disease.
In a retrospective review of over 7,000 cardiothoracic surgery patients, 14.5% developed perioperative heart failure.
This is similar to other studies, which have reported that IABPs are required peri-operatively in 8-12% of cardiac surgical patients.
Factors shown to increase the likelihood of perioperative heart failure are age, preoperative serum creatinine, and an associated mitral valve procedure.
Atrial fibrillation after surgery is associated with increased morbidity and mortality.
It is associated with increased length of ICU stay, perioperative infarction, persistent congestive cardiac failure and stroke.
There is a significant increase in in-hospital (5.95% vs. 2.95%) and 6-month (9.36% vs. 4.17%) mortality in patients with postoperative AF versus those without.
Postoperative bleeding and transfusion is associated with increased cost, increased infections and increased mortality.
Hazard ratios for mortality for patients requiring transfusion are 6.69 (95% CI 3.66 – 15.1) for 0 -30 days and 2.59 (95% CI 1.68 – 4.12) for 31 days to 1 year.
As is the case with all hospitalizations, the development of AKI indicates a patient is at increased risk of long-term mortality versus non-AKI patients.
This risk of mortality increases with increasing severity of injury.
The overall mortality for patients with AKI post bypass is 14% vs. 1% of those who do not develop AKI.
The mortality for those who require dialysis is 28%.
The mortality for patients with peri-operative heart failure is 13.5% versus 1.9%.
The necessity for IABP insertion is associated with increased mortality.
Mortality is 18.8 – 19.6% for preoperative IABP insertion, 27.6 – 32.3% for intraoperative insertion and 39 – 40.5% for postoperative insertion.
Special considerations for nursing and allied health professionals.
What's the evidence?
El-Chami, MF, Kilgo, P, Thourani, V. “New-onset atrial fibrillation predicts long-term mortality after coronary artery bypass graft”. J Am Coll Cardiol. vol. 55. 2010 Mar 30. pp. 1370-6. A retrospective review of the impact of AF on over 16,000 patients following CABG.
Kowey, PR, Dorian, P, Mitchell, LB. “Vernakalant hydrochloride for the rapid conversion of atrial fibrillation after cardiac surgery: a randomized, double-blind, placebo-controlled trial”. Circ Arrhythm Electrophysiol.. vol. 2. 2009 Dec. pp. 652-9. The randomized trial examining the efficacy of the novel anti-arrhythmic vernakalant in post-cardiac surgery AF.
Murphy, GJ, Reeves, BC, Rogers, CA. “Increased mortality, postoperative morbidity, and cost after red blood cell transfusion in patients having cardiac surgery”. Circulation. vol. 116. 2007. pp. 2544-2552. A paper detailing the morbidity and mortality associated with transfusion.
Chertow, GM, Levy, EM, Hammermeister, KE. “Independent association between acute renal failure and mortality following cardiac surgery”. Am J Med. vol. 104. 1998. pp. 343-348. Evidence of the long-term impact on mortality of AKI post surgery.
Kleinknecht, D, Jungers, P, Chanard, J. “Uremic and non-uremic complications in acute renal failure: evaluation of early and frequent dialysis on prognosis”. Kidney Int.. vol. 1. 1972. pp. 190The paper determining that early dialysis decreases mortality in renal failure.
Meyer, MM. “Renal replacement therapies”. Crit Care Clin. vol. 16. 2000. pp. 29An excellent review of renal replacement options.
Krawczeski, CD, Goldstein, SL, Woo, JG. “Temporal relationship and predictive value of urinary acute kidney injury biomarkers after pediatric cardiac surgery”. J Am Coll Card. vol. 58. 2011. pp. 2301-2309. Investigates the utility of a number of novel biomarkers to aid diagnosis of acute kidney injury in a pediatric cardiac surgery population.
Devarajan, P. “Update on mechanisms of ischemic acute kidney injury”. J Am Soc Nephrol. vol. 17. 2006. pp. 1503-1520. A description of pathophysiological processes underlying AKI.
DiDesa, VJ. “Pharmacologic support for postoperative low cardiac output”. Semin Thorac Cardiovasc Surg. vol. 3. 1991. pp. 313An excellent review of drug therapies for inotropic support in low cardiac output.
Fowler, MB, Alderman, EL, Oesterle, SN. “Dobutamine and dopamine after cardiac surgery: greater augmentation of myocardial blood flow with dobutamine”. Circulation. vol. 70. 1984. pp. 1103A comparison of the hemodynamic effects of dobutamine versus dopamine post cardiac surgery on coronary perfusion.
Ranucci, M, Ballotta, A, Castelvecchio, S. “Perioperative heart failure in coronary surgery and timing of intra-aortic balloon pump insertion”. Acta Anesthesiol Scand. vol. 54. 2010. pp. 878-884. A retrospective study of 7,270 patients who underwent cardiac surgery and evaluation of incidence of low cardiac output as well as treatment and outcomes.
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