The cardiothoracic ICU team provides care to patients following cardiothoracic surgical procedures. These include patients having traditional cardiac (CABG, valve replacements) via median sternotomy as well as minimally invasive (CABG, valve replacements) via a mini-thoracotomy. There may also be patients that required mechanical circulatory support devices such as Impella, IABP and ECMO. The scope of the care delivered includes support of all organ systems, invasive monitoring, ventilatory support, pharmacologic intervention, nutritional therapy, infectious disease management, and others.
The CVICU service is composed of an Attending (CCM or Anesthesia), an Advanced Practice Provider, and at times a critical care fellow working closely together with the cardiac surgical team to ensure the best possible care for each patient.
Expectations for fellows and Advanced Practive Providers: PLEASE READ CAREFULLY
1) Fellows/APPs will be expected to read the entire handout online by the first day of the rotation.
2) Fellows/APPs are expected to have in depth knowledge of every one of the pts they are following, including the following for each patient:
- Date and type of operation including valve replacement vs. repair/ prosthetic vs. biological
- Left and right ventricular function pre- and postoperative (as per TEE, generally found in OR records)
- Perioperative complications
- Home medications
- Preoperative/postoperative cardiac rhythm
- Significant past medical history
- Date of insertion of all lines
- The reason for every medicine on the EMR. For vasopressors, “septic shock” or “to counteract vasoplegia from propofol” is a better answer than “hypotension”
- The reason for every antibiotic (prophylactic, empiric, etc.), the reference culture data and the stop date
- Duration of spontaneous breathing trial the day prior and the marker of failure (RR, desaturation, tachycardia.)
- A list of any/all postoperative complications/procedures (pneumonia, reintubation, ARF, GI bleed, Afib, upper extremity DVT, cardioversion…)
- The pt’s current active diagnoses. Respiratory failure, hypotension and renal failure are generally inadequate descriptors. Pneumonia and volume overload causing respiratory failure, persistent hypotension due to sepsis and ARF due to interstitial nephritis are appropriate Dx.
3) Fellows/APPs are expected to sign out all of this information to the new fellow/APP at the time of service switch. The fellow/APP coming on service is responsible for getting this sign out. Fellows/APPs should not have to get the above information from the chart. Fellows/APPs should be getting this data from their peers. At the end of the rotation, please find out who is going to be taking care of the pt the next day and sign them out in full. Your obligation for care of the pt ends only then.
4) Full barrier protection for all central lines and arterial lines: aseptic hand washing, hat, mask, gloves & gown.
5) Fellows/APPs are expected to present patients each morning. The general approach of presentations should be:
- Neuro: “intubated and sedated” is not an adequate descriptor, a neuro exam must be done off of sedatives unless the patient is still paralyzed
- Cardiovascular: incl rhythm, hemodynamics, drips and plan
- Respiratory: incl CXR, duration of previous day’s weaning, secretions, volume status, US findings (A vs B vs A/B or C profile).
- Renal (volume assessment, labs, diuretics, ultrafiltration)
- Hematologic (presumed causes of thrombocytopenia, leukopenia)
- ID (including diagnoses, WBC, fever, new cultures, abx start and stop dates)
- GI (including abd exam, form of enteral access, calorie delivery)
- Endocrine (including need for adjusting insulin)
- A description of all lines and tubes along with output and insertion date
- Medications with plans for adjustment based on changes in dialysis method, renal function
6) Implementation of the daily care plan for each patient as established during morning rounds. Amendment of the plan as warranted with communication to the CCM attending and cardiac surgical team.
7) Routine orders – Lab testing should be based on the lab data required for management or diagnostic reasons.
8) ‘Routine” consults do not exist. Discuss plans for consultation with the CCM attending first. Specific physicians may be used preferentially. Also, it is best to speak with the CCM attending before pursuing diagnostic or therapeutic interventions suggested by a consultant.
1. To gain knowledge of the routine care and complications following coronary artery bypass grafting, valvular, and thoracic aortic surgery.
2. To gain introductory knowledge of the indications, complications and routine care of temporary mechanical circulatory support devices including: IABP, Impella device, TandemHeart, and ECMO.
CVICU: The fellow and the APP are expected to divide the service equally (if a resident is present then divide amongst the three members). The fellow/APP on service is expected to have knowledge of the patient’s progress on rounds and to present the data as well a plan for each active problem. Rounds in the CVICU begin at 7:00 am
Sign out of patients to both the Critical Care Attending and the on-call Advanced Practice Provider is done at 7PM by the attending covering the service.
Fellows/APPs MUST call the CCM attending for ALL new significant deteriorations. For guidance purposes this would include ALL of the following:
- New onset oliguria not responsive within 1 hour to fluid challenge.
- New loss of motor function, seizures or encephalopathy.
- Deterioration of cardiac index to less than 2.2 l/min/m2 not responsive to volume challenge within 30 minutes.
- New or worsening hypotension not responsive to volume challenge within 15 minutes OR requiring new or significant escalation of vasopressors.
- New significant bleeding (chest tube, GI, respiratory, etc).
- Worsening of gas exchange requiring significant escalation in FiO2 or PEEP.
- All major changes in patient condition MUST also be reported to the cardiac surgical team as soon as possible. Notifying surgical house staff does not obviate the need to contact the CCM attending.
1. Insulin infusion: aim to keep glucose control less than or equal to 180mg/dL
2. Heparin protocol:
- Stroke/VAD/High Risk Bleeding: Target 55-75 seconds. Aimed for early post-operative patient whom over anticoagulation has high risk of major bleeding. Once bleeding risk is decreased, use the Post-operative Protocol.
- Post-operative/AFib: Target 65-95 seconds. Used for post-operative patients with some increased risk of bleeding. This is the standard protocol for most CVICU patients. This protocol may be implemented with or without a bolus.
- Acute Coronary Syndrome: Target 55-75 seconds.
- DVT/PE: Target 65-95 seconds.
3. Electrolyte Replacement Protocol: Potassium, magnesium, and phosphorus replacement.
4. Spontaneous Awakening Trial: Ensuring sedation gets stopped and neurological assessment is done.
5. Spontaneous Breathing Trial: For the acute protocol the goal is to get postoperative patients extubated as soon as they have recovered from anesthesia (within 6 hours) and have no other active issues. For the chronic ventilator weaning trials either CPAP 5/PS 5 or trach mask should be used alternating with full rest. These daily spontaneous breathing trials (SBT) should be coupled with daily spontaneous awakening trial (SAT).
CARE OF THE CARDIAC SURGICAL PATIENT
I Postoperative Hypertension
Numerous factors can be responsible for post-op hypertension including chronic hypertension, sympathetic discharge secondary to pain and anxiety, agitation during emergence from anesthesia, rebound from b-blockade or preoperative antihypertensive agents, discomfort from the ETT/ventilator, hypoxia, hypercarbia, hemodilution or inotropic/vasoactive medications required in the O.R.
Excessive blood pressure can endanger suture lines on aortocoronary grafts and aortic cannulation sites and promote bleeding in the chest. For this reason:
Mean arterial blood pressures (MAP) are maintained under 80 mmHg in the first 12-24 hours post-op and SBP is strictly kept below 130mmHg.
If there is significant postoperative bleeding or concerns about suture line or cannulation site, the MAP may be maintained at 60-70mmHg (if directed by the surgeon and CCM attending).
TREATMENT of hypertension depends on the postoperative time frame. In the immediate postop period, the patient may be hypertensive but still fully sedated. In this setting nicardipine or sodium nitroprusside (NP) may be used. Nicardipine is the most commonly used antihypertensive in the CVICU due to its safety profile, particularly in patients with end-stage renal failure in whom nitroprusside toxicity is a concern.
Alternative vasodilator infusion used for hypertension is nitroglycerin. Nitroglycerine is preferred over nicardipine or nitroprusside if myocardial ischemia is suspected or if the heart was not completely revascularized. It is generally ineffective for severe hypertension. ACE inhibitors, hydralazine, calcium channel blockers, b-Blockers, or other longer acting antihypertensives which the patient may have been on preoperatively are considered preferable to the above infusions when the patient’s hemodynamic status stabilizes around 24 hours post cardiopulmonary bypass (CPB). Patients with recent MIs and EF>40% should preferentially be started on B-blocker therapy on POD 1 unless there is a contraindication. Pt’s with HFrEF should be started on GDMT with BB and an ACEI or ARNI unless contraindicated.
B-blocker therapy may also be a rare option in the immediate postoperative period in hyperdynamic patient (cardiac index >3.5) with tachycardia, hypertension, and normal ventricular function. However, CPB causes a predictable ventricular dysfunction, particularly in the first 8 hours post-op. Ventricles with pre-op low ejection fractions or wall motion abnormalities being particularly prone to dysfunction of greater severity and duration than normal ventricles (Mangano 1985). Because of the potential for myocardial depression, extreme caution must be used in initiating B-blocker therapy especially if the preoperative LV function was abnormal. Esmolol is preferred if used in the first 12 hours post-op. However, if any rule can be generalized for these patients:
avoiding negative inotropes such as B-blockers and verapamil in the first 12 hours following cardiopulmonary bypass cannot be overemphasized.
Metoprolol (12.5-25mg PO BID) is begun on POD #1 on most patients as prophylaxis against atrial fibrillation.
Although it may seem ludicrous to even mention this, it nonetheless bears repeating…. Do Not begin beta blockers on any patient still on continuous infusion of beta agonists/inotropes such as dobutamine, dopamine, epinephrine or milrinone.
If the patient still remains affected by neuromuscular blockade but is emerging from anesthesia, one of two options is appropriate: a) reversal of n-m blockade with neostigmine 2.5mg and glycopyrolate 0.6 mg or Sugammadex 2-4mg/kg (expensive) with intent to extubate, or b) the judicious use of fentanyl for further sedation. Restless, awakening, hypertensive patients with high sympathetic tone may benefit hemodynamically from sedation, though our bias is to allow full awakening and extubation ASAP. This often results in excellent BP control of the sympathetically driven, awake, intubated patient.
Hypotension and/or Low Cardiac Output
In the postoperative cardiac surgery patient, maintenance of adequate perfusion pressure is important to assure adequate flow through newly placed bypass grafts. Myocardium supplied by an internal mammary artery graft is particularly vulnerable to decrements in perfusion pressure. In general, mean arterial pressures of 60-70 mmHg are desirable in the immediate postoperative period. Higher pressure limits (MAP 70-80 mmHg) may be desirable in the presence of significant preexisting hypertension, myocardial ischemia usually represented as ventricular arrhythmias, renal or cerebrovascular disease and in the elderly.
Cardiogenic shock is a state in which ineffective cardiac output due to a primary cardiac disorder leads to inadequate tissue perfusion manifested by clinical (AMS, cold/clammy, mottled, oliguria) and laboratory data (elevated lactate, elevated creatinine) of end-organ dysfunction. The clinical presentation is typically characterized by persistent hypotension (SBP < 90mmgh for > 30 mins) unresponsive to volume replacement and is accompanied by clinical features of end-organ hypoperfusion requiring intervention with pharmacological or mechanical support. The absolute amount of cardiac output that will provide adequate tissue perfusion varies for each patient and clinical situation. As a guideline, we will intervene if patients have cardiac indexes < 2.2 l/min/m2. Patients with an index below this are at increased risk for postoperative morbidity and cardiac death. This association is likely related to the underlying cardiovascular disease rather than causally related to low perioperative cardiac output alone, though this distinction has not been defined in the literature. Causes of low cardiac output are extensive and may result from abnormal preload, contractility, heart rate, or afterload.
A. Decreased left ventricular preload
- Hypovolemia (bleeding, volume depletion, vasodilation from warming, vasodilators, narcotics, sedatives)
- Cardiac tamponade
- Positive pressure ventilation and autoPEEP
- Right ventricular dysfunction (RV infarction, pulmonary hypertension)
- Tension pneumothorax
- Abdominal compartment syndrome
B. Decrease contractility
- Low ejection fraction
- Myocardial “stunning”, ischemia or infarction
- Poor intraoperative myocardial protection
- Incomplete myocardial revascularization
- Anastomotic stenosis
- Coronary artery spasm
- Hypoxia, hypercarbia, acidosis
C. Tachy – and bradyarrhythmias
- Tachycardia with reduced cardiac filling time (particularly in patients with Grade I and II DD)
- Atrial arrhythmias with loss of atrial contraction (particularly in Grade I DD).
D. Increased afterload
- Fluid overload
E. Diastolic dysfunction (a common finding after cardioplegic arrest (J Thorac Cardiovasc Surg, 1997)
Syndromes associated with cardiovascular instability and hypotension
- Sepsis (hypotension from a reduction in SVR; hyperdynamic early and myocardial depression at a later stage)
- Anaphylactic reactions (protamine, blood products, and drugs)
- Adrenal insufficiency (esp. if patient on preoperative steroids)
Postoperative hypotension is most commonly related to hypovolemia or vasodilation with myocardial dysfunction and cardiac tamponade coming in a distant 3rd and 4 rd. Less common causes of hypotension include tension pneumothorax, protamine reaction, an inaccurate arterial line, overdoses of vasodilators or excessive intrathoracic pressure due to pulmonary hyperinflation and PEEP. The most important tools that you will use to differentiate these etiologies are:
1. History obtained at the time of transfer to the CVICU
2. New hemodynamic/perfusion assessments
History should be obtained at the time of transfer from the anesthesiologist. The most useful data will help you over the next 8-12 hours to form the basis of your “prior probabilities” from which you will interpret subsequent hemodynamic data.
- What was RV and LV function like at the start and end of the case (by TEE)? Is the LV wall thick and require higher filling pressures (h/o HTN or AS)?
- Was there ischemia by EKG or by wall motion change? If patient on NTG infusion from OR, suspect yes.
- Was inotropic support necessary for separation from CPB?
- Was clinical coagulopathy present during the case? If platelets given, suspect yes.
- In patients with poor postoperative CI, was baseline CI at start of the case normal?
The usefulness of history:
Inadequate RV inotropic support or RV overdistension would be the first considerations in the setting of pre-existing RV dysfunction, a rising CVP, and low BP/PCWP/CI.
In a patient with coagulopathy and nl RV function, the same hemodynamic assessment would strongly suggest cardiac tamponade.
Post CPB cardiac dysfunction causing elevated filling pressures, low CI and requiring inotropes is common in the setting of pre-existing LV dysfunction. It requires titrated management of inotropic agents and little if any further evaluation.
Post CPB cardiac dysfunction rarely causes a low CI requiring inotropes in the setting of normal LV function. The need for inotropes in this setting requires diagnostic evaluation to exclude ischemia or tamponade.
Hypertrophic LV cavities may still be underfilled echocardiographically with PCWP of 18 and a low CI, in this setting continued volume loading may still be indicated.
In patients with preoperative CIs <2.2 l/min/m2, a post-CPB CI goal >2.2 l/min/m2 may not be appropriate or achievable.
The first step in managing hypotension is to assess the physiologic derangement. If the patient is hypotensive, what is the cause?
underfilled and hyper-dynamic LV and RV cavities with small collapsible IVC
Variable, typically looks like hypovolemia with hyper-dynamic ventricles and small IVC.
LVOT VTI will be normal or high (> 20cm/s)
-If systolic failure: adequate LV filling with poor LV function.
LVOT VTI < 20cm
-If diastolic failure: small LV cavity often with thick ventricle, nl LV systolic function and low mitral e’ velocities, high E/e’
-hypokinetic and dilated RV with under-filled LV
-septal flattening and dilated IVC.
nl systolic function
-localized clot impairing cardiac filling
-ventricular interdependence and mitral inflow variation >25%
Preferred treatment in most cases
– PRBC if Hct <24, Hb less than 8 g/dL
-LR bolus 5mL/kg IV X 1-2 if Hb above 8 and CVP less than 8mmhg.
Dobutamine or Milrinone (If BP ok)
Epinephrine (if BP low)
Dopamine (if BP low)
Nitroprusside (if failure 2/2 high afterload)
-Mechanical Support (Impella, IABP, ECMO)
Maintain systemic BP with NE and avoid tachy-arrhythmia.
Inotropic support with Milrinone or Dobutamine
– Afterload reduce with Inhale NO or Veletri
-Diuretics (typically) vs Fluids (acute RV infarct) is pt specific and done under echo guidance
avoid vasodilators as well as sedation and intubation if possible. Vasodilation and positive pressure will likely cause patient to arrest.
Albumin 5% 250ml X 1-2 doses
Note: Check SVO2 if it is believed that the CI is unreliable (e.g. tricuspid regurgitation underestimates CI, or right to left shunt- overestimate CI).
Perfusion and Exam Assessments (Do I believe the cardiac index as a marker of adequacy of perfusion?):
1. Morbid obesity: CIs are typically lower than 2.2 l/min/m2 with acceptable perfusion.
2. Urine output: generally, > 0.5 ml/kg/hr:
- If low->suggestive of low perfusion (in absence of significant renal insufficiency or diuretic dependence).
- If nl or high-> suggestive of adequate perfusion though use of mannitol and high dose diuretics intraop can result in adequate urine output despite marked clinical hypoperfusion.
3. Mottling, livido reticularis: suggests hypoperfusion and a low CI.
4. Cool extremities, slow capillary refill (>3sec in hands, >5-7 secs in feet): suggests hypoperfusion of extremities though may be abnormal due to vascular disease.
5. Blood pressure: normal blood pressure in no way implies normal perfusion. It is not uncommon for patients to be in cardiogenic shock with acceptable BP.
The most frequent etiology of both low cardiac index and low blood pressure. Check cardiac index, CVP and PCWP; if all low–> volume challenge or resuscitate with pRBC (if Hb less than 8) until either:
- CVP rises (> 8-12 mmHg) but BP/PCWP/CI low–>suggests RV failure or localized tamponade
- CVP (>8-12) & PCWP (≥ 12 mmHg) rise but BP/CI low–>suggests LV dysfunction or possible tamponade
- CI rises (CI ≥2.6 l/min/m2) but CVP, PCWP and BP remain low–> vasodilation is the etiology
- BP and CI rise to an acceptable level even if PCWP and/or CVP remain low
As a guideline, resuscitation with blood is performed if ongoing bleeding or if the hemoglobin <8g/dL or Hct< 24. However, the decision to transfuse should be based on the hemoglobin, degree of ongoing blood loss, comorbid diseases, cardiac reserve and prior transfusion history not on an absolute trigger solely of the hematocrit being < 24%. An elderly patient with limited cardiac reserve and concomitant cerebrovascular disease may require transfusion at hemoglobin levels >8 g/dL. Conversely, healthier patients often have enough cardiac reserve to compensate for a lower red cell mass and tolerate hemoglobin levels well below 8 g/dL.
In the postoperative cardiac surgery patient, a state of normovolemic anemia often exists. Operative blood loss is replaced by colloid or crystalloid resulting hemodilution. This state is generally well tolerated, and hemoglobin levels progressively rise during the postoperative period as fluid is mobilized and diuresis occurs. These patients may receive no blood products during their surgery. In such patients who have not yet received blood and who have marginal indications for transfusion, it is appropriate to discuss transfusion with the surgeon and CVICU attending.
Decreased peripheral vascular resistance may be caused by medication, sedation, overdose of vasodilators or rewarming. Vasodilation is not uncommon post CPB, particularly in patients who have received antibiotic prophylaxis with vancomycin (Crit Care Med. 21:1124, 1993). Cardiac filling pressures are generally low and the BP often responds only transiently to volume.
Inappropriate vasodilation can be diagnosed in every patient who has hypotension despite an adequate cardiac index.
The management generally consists of early use of norepinephrine or phenylephrine rather than repeated volume challenges if the cardiac index is ≥2.6l/min/m2, urine output >0.5cc/kg/min, and perfusion on physical exam is adequate.
Because the management strategy of low CI/low CVP (hypovolemic) patients differs from nl/high CI/low CVP (vasodilated) patients, cardiac outputs are performed as frequently as needed to distinguish these “dry appearing” populations.
If the BP of a vasodilated patient becomes more labile and less responsive to norepinephrine, urine output decreases, or CI drops to <2.6l/min/m2, further volume challenges with reassessment of hemodynamics is warranted.
Acute tamponade requires immediate surgical intervention. If clinical suspicion exists, rapid diagnosis and treatment take priority. Tamponade usually results from the accumulation of blood and clot in the mediastinum. Tamponade may present insidiously, often in stages until a precipitous drop in cardiac output occurs. As blood and/or clot accumulate, diastolic filling in progressively impaired resulting in a decreased stroke volume. As preload is reduced, a compensatory tachycardia may ensue with rising CVP and RA pressures and hypotension. Hemodynamic collapse occurs soon after.
In the setting of preserved ventricular function ± excessive bleeding, a falling cardiac output and CVP of 18 is suspicious for tamponade. The lack of supportive mediastinal widening by CXR, low ECG voltage or “diastolic equalization of pressures” carries very little weight in ruling out the diagnosis. Myocardial compression in this setting may involve thrombus restricting filling of a single cardiac chamber.
TEE is the imaging procedure of choice in suspected tamponade. TTE may show RA systolic collapse, RV diastolic collapse with a dilated IVC, increase tricuspid (>40%) and Mitral (>25%) inflow (E) variation, however, keep in mind that surgical tamponade can occur with a localized clot compressing only the LA and without a circumferential effusion, for this reason TEE is the image modality of choice, CT scan of the chest can also show the extent and location of a pericardial effusion.
Tamponade must be considered in any patient with worsening low output and increasing pressor/inotrope requirements in the first 12 hours postoperatively.
It is highly unlikely that a patient has cardiac tamponade if they are still requiring nicardipine for hypertension control.
Definitive treatment is surgical evacuation of blood or clot. Hemodynamic management prior to operative therapy includes fluids and vasopressors. If the patient is breathing spontaneously, avoid placing on positive pressure ventilation unless absolutely necessary as this may further reduce cardiac filling and lead to cardiac arrest. If the patient is already intubated strongly consider decreasing PEEP.
Dysfunction of the LV and/or RV in the postoperative period is marked by a low cardiac index, adequate filling pressures and evidence of hypoperfusion clinically. Although the list of potential causes is long, the major reasons are outlined below.
Functional myocardial depression (from cardiopulmonary bypass): Well described impairment of ventricular function occurs after CPB. In normal hearts, the 20% decrement in function is clinically unapparent and readily reverses within 4-8 hours. In sick hearts (LVEF<45% or wall motion abnormalities), a decrement of 40% in LV and RV function occurs post CPB and only approximately 50% of this deterioration has been reversed 24 hours postoperatively (Anes.62:571,1985).
Inadequate myocardial protection: Technical and anatomic factors may limit the efficacy of cardioplegia such as a hypertrophied ventricle or the presence of a patent LIMA in a patient undergoing redo CABG. Ventricular function may suffer in the postoperative period.
Perioperative infarction (POMI): Patients with ongoing ischemia necessitating emergent CABG are at very high risk of postoperative myocardial dysfunction which often times is severe. In clinically insignificant cases, the use of ST or T wave changes are notoriously nonspecific for infarction because normal perioperative changes (hypothermia, electrolyte changes and pericardial inflammation) can affect these components. Since cardiac enzymes are elevated in most postoperative cardiac surgery patients, their value in establishing a diagnosis of POMI, especially if small, is substantially inferior to a medical population. Because of these limitations and since patient management is generally not affected by clinically insignificant POMI, the diagnosis is not aggressively pursued in this setting.
Graft compression: Usually recognized before leaving the OR. Patients generally have ECG changes or new wall motion abnormalities present on TEE. Treatment involves revision of graft in most cases.
Coronary vasospasm: ST elevations have been found in 8% of Holter monitors in the first 12 hours after CABG (Chest.89:647,1986). Only 1% of patients have clinically evident spasm and 50% of these present while the patient is still in the OR. Postoperative ECG ST elevations in the distribution of a new graft may be the only sign though hemodynamic instability or new wall motion abnormalities may be evident on TEE. Response of the ECG changes to nitroglycerine is marginal. The majority of patients are successfully treated with nifedipine which should be considered even in the setting of hypotension. Response to nifedipine is considered highly suggestive that spasm was the etiology. Administration of one gram of calcium chloride (via a central line) may counteract the hypotensive effects of nifedipine in this setting. A calcium antagonist in combination with NTG is more potent than calcium antagonist alone or NTG alone in prevention of human RA vasospasm after coronary bypass (Ann Thorac Surg, 2000).
Graft occlusion: Occurs in 10% of saphenous vein grafts in the first month and may be immediate. Again, new ST elevations may be the only finding. If the patient is hemodynamically unstable or the area of myocardium at risk is particularly vital (e.g. LAD distribution or the inferior-lateral wall in a patient with a previous AWMI), graft revision would be strongly considered. It is critical to inform the surgeons of new ST elevations on the ICU admission ECG, especially those ≥ 2 mm. They will have the best insight as to the significance of this finding given the patient’s coronary anatomy, the quality of the grafts, possibility of coronary emboli and will need to ultimately decide whether intervention is warranted.
Coronary air embolism: Typically evident on TEE in the OR and variably leads to myocardial dysfunction. Care is supportive and often managed by increasing coronary perfusion pressure. ECG generally resolves within a few hours.
Acute pulmonary hypertension: May precipitate RV failure in patients who do not have preexisting pulmonary HTN and conditioned right ventricles. Protamine reactions or severe acute lung injury due to blood transfusions and prolonged CPB are potential etiologies. The most feared protamine reaction is severe immediate pulmonary vasoconstriction which may lead to RV failure and cardiovascular collapse (Anes.59:470, 1983).
TREATMENT of HYPOTENSION and/or LOW CARDIAC OUTPUT
Treatment options for hypotension and/or low cardiac output may include volume and blood repletion, inotropic, chronotropic and vasoactive agents, cardiac pacing, antiarrhythmics, mechanical assist devices and agents to decrease oxygen consumption. Vasoactive agents typically used in the hypotensive postoperative cardiac patient include vasopressors such as norepinephrine and vasopressin, inoconstrictors: dopamine and epinephrine; as well as inodilators: dobutamine and milrinone. The choice of vasoactive therapy depends on the etiology of the hypotension, the cardiac versus peripheral effects and the potential side effects that may be incurred. The fellow/APP should discuss with the CCM attending the need for new vasoactive therapy or a significant escalation in the dosage.
For LV dysfunction associated with low CI (<2.2L/min/m2) and low BP (MAP <60 mmHg or SBP <90mmHg), low dose Epinephrine (0.03mcg/kg/min) or Dopamine starting at 3-5mcg/kg/min are often first choices once adequate preload has been assured. Although a PCWP of 12 mmHg may be acceptable before adding inotropes, higher filling pressures of 15-18 mmHg should be considered in patients whom continued volume challenges lead to continued improvement in CI. In patients with hypertrophied ventricles, a PCWP of at least 15-18mmHg should be assured before beginning inotropes since inadequate ventricular filling rather than systolic dysfunction is generally the culprit. Epinephrine and Dopamine provide both inotropic and vasoactive support, typically in a dose dependent fashion. Epinephrine may cause a lactic acidosis in some post-CPB patients (Crit Care Medicine 25:1693, 1997). Dopamine vasodilates coronary vessels and increases myocardial perfusion; therefore, it is reasonable well tolerated in hearts with residual ischemia unless tachycardia occurs. Any of these agents can act idiosyncratically causing an unacceptable degree of tachycardia. An IABP or an Impella device may be appropriate and should be considered early in a patient not responding well to titration of pharmacologic support.
For LV dysfunction associated with low output and normal BP, Dobutamine is generally our first choice. Dobutamine increases cardiac output and decreases cardiac filling pressures without a significant increase in myocardial oxygen consumption (unless tachycardia is present). Dobutamine is better than dopamine in matching increased coronary blood flow with increased cardiac output. Also, Dobutamine tends to lower systematic blood pressure as opposed to dopamine which usually raises pressure. In some cases, dobutamine maintains or raises systemic pressure. This may be seen in patients that are highly dependent on cardiac output to generate blood pressure. Indications to switch from Epinephrine/Dopamine to Dobutamine include ischemic ECG changes noted with escalation of infusion dose and unacceptable elevations in blood pressure or heart rate. Alternatively, a phosphodiesterase inhibitor such as milrinone may be used when LV dysfunction is coupled with low CI and normal BP. Milrinone increases cardiac output primarily by decreasing vascular resistance though there is evidence that an inotropic effect occurs particularly in ischemic myocardium (Ann Thor Surg.57:540,1994). Tachycardia is minimal but hypotension is common. Milrinone may also be useful in patients developing tolerance to dobutamine, and is less arrhythmogenic than any of the above mentioned agents.
RV dysfunction associated with low cardiac output and hypotension is not uncommon and can be exceedingly difficult to manage. Hemodynamic goals include maintaining systemic blood pressure, lowering RV afterload (PVR), treating absolute or relative bradycardias, and maintaining atrioventricular synchrony. Factors which contribute to post pump RV dysfunction are chronic pulmonary hypertension, acute pulmonary hypertension due to acute lung injury, LV diastolic dysfunction in the setting of chronic HTN or AS, RV overdistention in the absence of pericardial constraint, long pump runs with inadequate RV preservation and RV hypoperfusion due to factors such as right coronary air embolism or non-revascularized right CAD. A rising CVP (>18) in the absence of a corresponding increase in STROKE VOLUME (CO/HR) should raise the suspicion of RV dysfunction or tamponade. Another clue would be a CVP to PCWP ratio greater than 1. Although with primary RV dysfunction, PCWP would be expected to be low, a combination of LV diastolic dysfunction with RV dysfunction due to inadequate preservation may induce RV failure, in this scenario with a high PCWP. Echo-cardiographic evaluation is required.
Treatment consists of maintaining systemic blood pressure with Norepinephrine or low dose vasopressin followed by the initiation of inodilators such as milrinone or dobutamine. Afterload reducing agents such as iNO or iVeletri are commonly used for cases in which the PVRI is elevated. Inoconstrictors such as Epinephrine, Dopamine should be used with caution as they can precipitate tachy-arrhythmias, thus reducing RV filling. Avoidance of RV over-distention (CVP >20) to reduce RV wall tension is typically employed with the use of diuretics or ultrafiltration. That being said, the value of CVP deteriorates if significant TR develops. If RV failure is manifested before leaving the OR the chest may be left open. This delayed sternal closure prevents the hemodynamic collapse which occurs when the dilated RV is compressed during closure. The sternum is closed typically in 48-72 hours when the RV has recovered, and patient’s volume overload is reduced. Maintenance of atrioventricular synchrony is critical in the setting of RV dysfunction, cardioversion and amiodarone, as well as atrial pacing when possible, are often crucial in maintaining cardiac output in the setting of Afib or accelerated junctional rhythms.
In vasodilated patients (MAP <60 mmHg or SBP <90mmHg with a CI ≥2.6), Norepinephrine is our drug of choice. Phenylephrine and Vasopressin may be used as well. Caveats in the treatment of vasoplegia:
If BP and filling pressures are decreased-> CHECK CARDIAC OUTPUT! If the perfusion is acceptable on exam and CI ≥2.6l/m/m2 you should be thinking “increase vascular tone” not “fill the tank with another 6 liters”.
Reassess the cardiac index once you are on pressors. If CI has dropped to <2.6 l/m/m2, you should consider further volume challenge.
If there is evidence of hypoperfusion (decreasing urine output, cooling of extremities, etc) reassess the hemodynamics.
Be wary of radial artery lines to give accurate BP assessment as pressor requirements rise (phenylephrine > 1 mcg/kg/min, Epi/Norepi > 0.1 mcg/kg/min). Have a low threshold to place a femoral arterial line to avoid excessive alpha agonists if they are not needed. Escalating pressor requirements for vasodilation in the absence of a concomitant rise in cardiac index should alert you to this possibility.
Before ordering a new vasopressor or inotrope, check and see what drips are already hanging but not running at the patient’s bedside. If you seek inotropic support and choose Dobutamine, try first using the Epinephrine or Dopamine that is already on the patients EMR from the OR. There is no added cost and, in many cases, will work just as well as the Dobutamine.
Calcium is a potent inotropic agent in hypocalcemic patients or in those with a decreased ionized fraction of calcium. Low ionized calcium can occur postoperatively from citrate infusion during blood transfusion and during periods of alkalosis. In the O.R., calcium is often used during weaning from cardiopulmonary bypass. Postoperatively, calcium may be used to reverse myocardial depression due to calcium channel blocker-enriched cardioprotection solution, halogenated anesthetics and hypocalcemia. Appropriate use of calcium in myocardial depression increases cardiac output and blood pressure without increasing heart rate. In response to low post-CPB ionized calcium, 1 gm of calcium chloride should be given via a central line. Calcium should be administered with caution in all cardiac surgery patients as it can cause coronary artery graft spasm and can potentiate the effects of digitalis toxicity and hypokalemia. Overzealous administration of calcium after the ionized fraction is normalized can reportedly result in SVT.
POSTOPERATIVE BRADYCARDIA and CONDUCTION DEFECTS are common due to intraoperative use of b-blockers, cardioprotection solution enriched with a calcium channel blocker, sinoatrial ischemia, conduction system ischemia and edema, cardioplegia, electrolyte abnormalities, sympatholysis or preoperative conduction disturbances. Conduction defects in descending order of frequency include RBBB, left anterior hemiblock and incomplete RBBB. With the possibility of postoperative heart block and arrhythmia, epicardial pacer wires are placed prior to chest closure. You must learn if the cardiac surgeon that performed the operation places ventricular and atrial wires or just ventricular wires routinely. Atrial pacing when available, best supports hemodynamics during sinus-bradycardia and junctional rhythms. It also decreases the number of premature atrial and ventricular depolarizations. Ventricular pacing is most useful in optimizing heart rate during AV dissociation and atrial fibrillation with slow junctional rhythm. Two potential problems can occur during lone ventricular pacing; loss of AV synchrony and abnormal ventricular activation resulting in inefficient contraction with decreased stroke volume. In the former, the atria contract against closed AV valves resulting in decreased stroke volume and increased mean atrial pressures. Most postcardiotomy patients have better cardiac outputs and blood pressure with a sinus bradycardia at 58 than a ventricular paced rhythm at 90, particularly if the ventricular function is impaired or if the left ventricle is hypertrophied. It is worth trying ventricular pacing in the setting of sinus bradycardia or a junctional rhythm to assess whether it will have a beneficial effect on CI and BP though the success rate is quite low. A catechol infusion of epinephrine (0.05 mcg/kg/min), Dopamine (5 mcg/kg/min), or Dobutamine (5 mcg/kg/min) titrated to heart rate will often be more helpful.
ACCELERATED JUNCTIONAL RHYTHMS may be benign or may cause hemodynamic chaos in patients with impaired LV function, impaired RV function (e.g. RV infarct), and noncompliant, thick LVs (i.e. AS, severe hypertension). These patients may occasionally be in shock in the postcardiotomy period due to an accelerated junctional rhythm. Additional inotropes may support the CI in patients with dysfunctional ventricles and additional volume in patients of hypertrophic ventricles until an atrial kick returns. If these conservative measures fail, a transvenous atrial pacing wire should be considered.
SUPRAVENTRICULAR TACHYCARDIA, which include sinus tachycardia, atrial fibrillation, atrial flutter and reentrant SVT are the most common supraventricular tachyarrhythmias.
Sinus tachycardia may be caused by hypovolemia, anemia, pain, rebound from b-blocker, hypoxia, EtOH withdrawal, hypercarbia, and fever, endogenous or exogenous catecholamines. Heart rates >110/min can generally be successfully addressed with:
Volume (if hypovolemic).
Decreasing or changing catechol infusions.
Fentanyl (50-100mcg) if hypertensive and emerging from anesthesia. If sinus tachycardia is a manifestation of a hyperdynamic state (tachycardia with a high cardiac output and high BP), b-blocker therapy may be indicated as previously discussed though with great reservation in the first perioperative hours.
New onset atrial fibrillation (AF) occurs in 30-40% of postcardiotomy patients within the first 3-5 days after surgery. The increased frequency of AF in postoperative CABG and valvular surgery patients is attributed to pericardial or mediastinal inflammation, atrial distention and hypoxemia. Its occurrence during the early postoperative period (12 hr) is infrequent. Additionally, it is not unusual for patients in chronic AF to return from the O.R. in sinus rhythm; however, this is short-lived and atrial fibrillation returns within the first few hours postoperatively.
In all patients:
Minimize adrenergic stress – mechanical ventilator support if high work of breathing/respiratory failure; pain control.
If hypoperfusion (cool, clammy, mottled, hypotensive or angina), ensure adequate analgosedation and proceed with synchronized cardioversion beginning with 100j.
Atrial fib/flutter associated with critical illness will be recurrent as long as the patient remains critically ill; maintenance therapy should be instituted.
Optimize metabolic milieu (e.g. treat with additional magnesium and correct hypokalemia).
Rate control first if hemodynamically stable (HR goal <120), CCB/beta blockade alone may lead to conversion to NSR.
Reduce catechol infusions (epinephrine, dobutamine, dopamine) if possible
- Diltiazem 5mg IV over 5 minutes Note: CCB or b-blockers NEVER make sense if patient is on inotropes! Alternatively, an Esmolol bolus may be given
Amiodarone 150 mg load (OVER 30 minutes on a pump) then infusion at 1 mg/min.
Diltiazem infusion 5-20mg/hr.
Digoxin 0.5 mg IV (SLOW onset of action), then 0.25mg IV in 4 hrs and 8 hrs. If the patient has not been on digoxin previously. Digoxin not first line Rx
Goal is cardioversion to NSR unless h/o chronic atrial fibrillation or if patient is going to require anticoagulation for another reason. In those circumstances, rate control is appropriate.
Once rate < 120 with above therapies…
If without chronic lung disease: amiodarone 400mg PO TID x 4 days, then 200 mg po daily (hold digoxin since bradycardia occurs). IV dosing of 150mg over 10 minutes, then 1mg/min x6 hrs, then 0.5 mg/min X 18 hours significantly more expensive (hold if HR<65).
If preserved LV function and absence of active bronchospasm: sotalol 80 mg PO bid (decrease dose if renal disease or bradycardia); follow the QTc and if > 500msec hold drug and reduce dosage.
Procainamide 1000mg IV over 1 hr then Procan SR 12.5 mg/kg PO q6h (decrease if reduced renal function); if QTc <500msec in 24 hrs and atrial fibrillation persists, give additional 500mg over 30 minutes and increase PO dose by 250 mg q6h; HR must be controlled prior to Procan loading since conduction and ventricular response may be increased.
Synchronized cardioversion beginning with 100j if unstable or if nearing the 48h mark s/p onset of atrial fibrillation. Paroxysmal atrial fibrillation should be cardioverted only after augmenting antiarrhythmic levels or suppressing sympathetic stimulation.
Atrial flutter: more difficult to rate control but easier to convert
Synchronized cardioversion may be tried starting at 50j using appropriate conscious sedation (e.g. Etomidate 0.1 mg/kg, ketamine 0.5mg/kg).
If conversion to atrial fibrillation, try to convert as above starting with 100j.
If resulting atrial fibrillation recurs, treat with rate control and pharmacologic agents as above to convert.
If refractory or recurrent flutter, rate control with metoprolol, esmolol, diltiazem, or verapamil as above, then amiodarone, sotalol, procainamide as above.
Reattempt synchronized cardioversion after loading antiarrhythmics if patient remains in flutter at 48hrs.
If atrial pacing leads are present, consider rapid atrial pacing to convert.
If failure to convert, electrophysiology evaluation for radio-frequency ablation.
Treat underlying causes of sympathetic stimulus.
Rate control preceding cardioversion unless poor perfusion or angina.
Attempt pharmacological cardioversion early.
Consider synchronized cardioversion at 36-48hrs of onset, otherwise consider IV heparin protocol.
Premature ventricular complexes (PVC’s) may be associated with ischemia or hypoxia, electrolyte imbalance, high sympathetic tone, exogenous catechols, hypothermia, acid-base derangements and poor cardiac function. These factors provide the focus for evaluation. After evaluation and correction of the above, the decision to treat with antiarrhythmics is based on two considerations: the effect on hemodynamics and the potential threat of VT or VF. The decision to treat sustained unifocal PVC’s bigeminy or trigeminy that are not affecting the hemodynamic status is based on individual cases with particular focus on preoperative arrhythmia history, ventricular function, current level of inotropic support and the possibility of proarrhythmic drug effects. In the immediately perioperative period, significant new ventricular ectopy is managed with normalization of K+, additional MgSO4, followed by lidocaine. The lidocaine infusion should be decreased to 1mg/min at 8 hrs postop and be discontinued on morning rounds POD 1 typically. Levels don’t need to be followed unless there is a documented need to continue the drug for >12-18hours. Less than 1% of CABG patients require such antiarrhythmic therapy. Amiodarone and Procainamide are alternative agents if lidocaine is ineffective. Cardiac pacing above the intrinsic rate may also suppress ectopy.
In general, the treatment of ventricular tachycardia (VT) and fibrillation (VF) follows ACLS guidelines; however, there are some important aspects of intervention that are unique to the postoperative cardiac surgery patient.
***Closed chest CPR can cause SEVERE CARDIAC DAMAGE in patients with PROSTHETIC VALVES and RECENT STENOTOMY, in addition, anterior mediastinal chest tubes can be driven into the RV during CPR. The emphasis is on early defibrillation followed by OPEN CHEST and internal cardiac massage ASAP.
Cardiac arrest after cardiac surgery is managed differently than in ACLS. Prompt resternotomy within 5 minutes is emphasized given the list of potential reversible causes for which external cardiac massage is ineffective and may be harmful. For more information, please click on the link below. It is strongly encourage that you familiarize yourself with published guidelines and protocols before rotating through the unit.
–Refractory VT occurring in the early postoperative period can be caused by graft occlusion and usually prompts the use of open chest CPR and exploration of the mediastinum via the sternotomy incision. Also, this approach permits the use of internal defibrillator paddles if external defibrillation is unsuccessful. Recurrent sustained VT is occasionally responsive to overdrive pacing via epicardial wires.
A large number of patients presenting after cardiac surgery are elderly with significant comorbid disease such as diabetes or peripheral vascular disease with prior renal insufficiency. Subject these patients to CPB, alterations in hemodynamics and nephrotoxic agents and the stage is set for renal dysfunction. Risk factors for renal failure differ during the intraoperative and postoperative period. The intraoperative risks include hypotension, low CPB flow, the effects of deep hypothermic arrest and tubular damage from free hemoglobin or myoglobin. During the post-bypass and postoperative period; vasopressors, blood products, hypotension, low cardiac output and nephrotoxic drugs comprise the majority of risk factors.
The two major elements that initiate the evaluation of renal function are postoperative oliguria and rising BUN and creatinine levels. Normal to high urine outputs are the norm in the early post-CPB period since patients are almost universally exposed to mannitol from the CPB circuit ± loop diuretics intraoperatively. Also, hypothermia can induce a “cold” diuresis irrespective of volume status. Low urine production in the first 12 hours postoperatively overwhelmingly is a sign of hypovolemia, low output, low systemic BP, or decreased renal blood flow due to vasoconstriction. In subsequent hours, particularly in patients whom have been diuretic dependent preoperatively, diuretic therapy is often an appropriate response to oliguria after the above-mentioned hemodynamic factors have been assessed.
Respiratory Management following CPB
Cardiopulmonary bypass affects lung function, mechanics, blood flow and metabolism. During complete CPB, all systemic venous blood is diverted into the oxygenator and there is no blood flow to the right heart or pulmonary circulation. Extravascular lung water increases from a temporary alteration in pulmonary capillary integrity or in an increase in pulmonary hydrostatic pressure. Intrapulmonary shunting and increased dead space ventilation occur from increased lung water, atelectasis and changes in microcirculatory dynamics. Collectively, these cause inefficient matching of ventilation and perfusion. Increased dead space ventilation/perfusion mismatching results in an increase in A-a gradient and a decreased Pa02. Neutrophils are sequestered within the pulmonary microcirculation during CPB and release of neutrophil mediators may result in membrane damage, localized vasoconstriction and capillary occlusion. This phenomenon also contributes to extravascular edema and V/Q mismatching respectively.
Pulmonary vascular dynamics are also affected during CPB. Neutrophil sequestration and mediator release can affect the microcirculation. Also, the direct effects of CPB, hypothermia and vasoactive drugs can alter pulmonary vascular response to hypoxia and interfere with hypoxic pulmonary vasoconstriction. This can contribute to V/Q mismatching and a decreased Pa02.
Lung dysfunction ranges from mild decreases in Pa02 to profound respiratory failure resembling ARDS within the first 72 hours following CPB. Most patients exhibit some decrease in Pa02 in the immediate postoperative period and it is difficult to predict which patients will develop significant respiratory insufficiency. Factors associated with significant respiratory insufficiency include a bypass time >150 min, the amount of perioperative blood transfusions and postoperative ventricular function. Although there is no absolute degree of dysfunction that defines “significant” respiratory insufficiency, it is characterized by a progressive worsening of the CXR with decreasing pulmonary compliance and an elevated A-a gradient and shunt fraction.
Mechanical Ventilation Goals
In uncomplicated patients, mechanical ventilation is maintained until the effects of anesthesia and neuromuscular blockade have abated. In these patients, we prefer to liberate them from mechanical ventilation as soon as they are awake, moving and fulfill clinical criteria for extubation. In stable awake patients, there is no need to “wean” from mechanical ventilation. These patients can be changed directly from mandatory ventilation to PS/CPAP with rapid extubation if the clinical situation permits. We utilize protocols for liberating from mechanical ventilation based on oximetry saturations as well as hemodynamic and clinical parameters (i.e chest tube output).
The goals of mechanical ventilation extending beyond the early postoperative period include control of acid-base status, ability to apply PEEP, support of respiratory muscles during insufficient cardiac output, airway protection, pulmonary toilet, to aid in the control of hemodynamic instability, to permit a smoother return to the O.R. if excessive bleeding is present or to support the need for pharmacologic paralysis and sedation.
Postoperative hypoxemia is common and may be easily overlooked. Pulse oximetry sometimes cannot be used in the early postoperative period due to cold extremities and failure to sense. Also, patients often have a moderate respiratory alkalosis after arrival from the O.R. thus shifting the oxygen dissociation curve. iSTATs are obtained upon arrival to CVICU to assess p02, pC02 and acid-base status, Htc, Ionized calcium and K+ levels. Mechanisms for postoperative hypoxemia are listed below:
2) SHUNT (cardiac or pulmonary)
- vasodilators* (NTG or nitroprusside, etc.)
- neutrophil aggregation in microcirculation
- lobar collapse
- right mainstem ETT migration*
3) DECREASED MIXED VENOUS OXYGEN CONCENTRATION: the greater the shunt, the greater the effect of decreased MVO2 on arterial oxygenation
- increased oxygen consumption (shivering or sepsis)
- decreased cardiac output
- decreased Pa02
4) V/Q MISMATCH and DECREASED ALVEOLAR-CAPILLARY DIFFUSION
- cardiogenic pulmonary edema
- non-cardiogenic pulmonary edema
- protamine reaction
(*) = common causes
-Atelectasis is the most common cause of hypoxemia upon transfer from the OR. Manual recruitment in most cases resolves this issue and no further assessment is warranted.
-Nitroprusside commonly, even at low levels, may increase shunting in patients.
-Non-cardiogenic pulmonary edema following CPB is rare but striking in its presentation. Patients will often have reasonable initial gas exchange and CXR which deteriorates on POD 1, 2, or 3. The etiology is not known. In some patients, the presentation is more of a non-inflammatory capillary leak that responds to aggressive diuresis, supplemental O2, ±CPAP mask, ± mechanical ventilation for 48-72 hours. The alternative presentation is that of an inflammatory ARDS which does not respond to diuresis and requires aggressive ventilatory support and PEEP with substantial mortality.
Liberation from Mechanical Ventilation
During liberation from mechanical ventilation, there are no absolute numerical criteria that predict successful extubation. There are however, general criteria that should be considered prior to weaning. Patients should be normothermic, exhibit adequate neurologic function (awake, muscle strength, gag), and minute ventilation as well as be stable from a hemodynamic and hemostatic standpoint. In a patient who is marginal for extubation and has an IABP which is to be removed, we may choose to remove the IABP in the AM and extubate the patient 6 hours later. This is because the patient must remain flat to decrease the risk of developing a groin hematoma following IABP removal, and this supine period may be a substantial respiratory burden in a marginal freshly extubated patient. Sternotomy with IMA harvesting is accompanied by a greater impairment in pulmonary function than when vein grafts are used. This impairment may be due to the irritating presence of pleural chest tubes and more extensive chest wall manipulation. The type of grafts does not materially affect extubation nonetheless. Overwhelmingly, the goal is to promptly extubate patients when they have adequately recovered from anesthesia.
Post Extubation Care
After successful extubation, deep breathing, incentive spirometry, pain control, prompt chest tube removal to minimize splinting and early mobilization are the mainstays of therapy. More aggressive therapies such as NT suctioning, chest physiotherapy, IPPB, nasal CPAP/NIPPV and bronchodilator therapy may have a role in a small number of patients. Incentive spirometry is a must while awake and should be verbally reinforced at the bedside. Adequate pain control with oral narcotics or PCA are key to optimizing patients after extubation.
Pleural effusions after coronary revascularization are multifactorial in origin and may be caused by pericardial inflammation, atelectasis, transected lymphatics during mobilization of the IMA pedicle or inflammation from the physical presence of chest tubes.
Patients revascularized with an IMA routinely undergo left pleurotomy with subsequent chest tube placement. Vein grafts do not require left chest tubes unless the pleural space has been violated. Irrespective of the type of graft utilized, pleural effusions not caused by cardiac failure or volume overload occur predominately on the left. The decision to effect drainage is based on the clinical situation. Effusions that are asymptomatic, responsive to diuresis or are decreasing over time should not require drainage. Large effusions causing compressive atelectasis or dyspnea, potentially infected effusions or those hindering weaning from mechanical ventilation should be drained. In the latter case, large effusions must be present to cause a restrictive defect during pulmonary function testing; however, the sensation of dyspnea may hinder ventilator weaning.
Drainage is performed by either “pigtail” catheter or tube thoracostomy depending on the size, substance and location of the effusion. Bedside US must be done prior to chest tube insertion to evaluate position of the diaphragm, potential loculations, subpulmonic components, effusion size and accompanying atelectasis. Careful attention to diaphragm position will prevent subdiaphragmatic placement of the device. As always, pleural tubes should be inserted at or above the level of the nipple. Remember that the insertion site does little to determine the tip of the tube’s position (unless, that is, the needle pierces the ventricle or the lung parenchyma).
Chest Tube Management
During cardiac surgery, the type of procedure dictates the number and position of the chest tubes. All median sternotomy patients have a mediastinal tube placed to drain areas around the pericardium and mediastinum. A left pleural tube is required during internal mammary artery grafting as the left pleural space is opened. The right pleural space is generally not opened but may be entered inadvertently requiring tube thoracostomy. Chest tubes should be inspected upon arrival to CVICU for bleeding, proper function and to assure that connections are secure. In the presence of an air leak, an occluded tube can result in a tension pneumothorax. A common mistake is to allow the tubing to loop so that the effluent must flow upward for a length. If fluid collects in the upward limb of the loop to a height greater than the amount of suction, the tube is effectively sealed and functions as if it was clamped. Tubing must remain horizontal or descending.
Tubes and wires
We usually remove the mediastinal CT’s on post op day (POD) #2-3. However, for minimally invasive cases, even if drainage is minimal we still do not remove these tubes until POD#3. In these cases if serous drainage is more than 300 cc/day, the chest tubes will be left an additional day. All minimally invasive cases are placed on NSAID’s starting in the ICU (Toradol 15 mg IV q 8 hours X 4, then Motrin 200mg bid X 3 weeks). Patients who have a history of coronary artery disease, excessive post-op bleeding or renal insufficiency (Creatinine >1.4) should NOT be started on NSAID’s. Pleural chest tubes are removed once output is less than 200 ml/day with no air leak and no pneumothorax.
- Temporary pacing sensitivity and capture thresholds should be checked daily
- If platelets are >75 and INR <1.4, pull pacing wires on POD #2-3 or later at discretion of surgeon unless contraindicated for other reason (rhythm, advanced age, known friable tissues due to steroids, etc)
- Cut pacing wires only with staff surgeon approval
A CXR is unnecessary after chest tube removal unless the patient becomes symptomatic or there is clinical evidence of pneumothorax. If there was a recent air leak, check a chest radiograph the next morning. If a pleural and mediastinal tube are “Y” connected, the mediastinal tube can be clamped before removal to maintain the integrity of the pleural conduit.
Phrenic Nerve Dysfunction
Phrenic nerve injury causing diaphragm dysfunction ranges from transient diaphragmatic paresis resolving within the immediate postoperative period to permanent bilateral paralysis. Causes include local hypothermia during cooling of the chest cavity, subclavian and internal jugular venipuncture, mediastinal manipulation and sternal retraction.
Clinically, unilateral diaphragm dysfunction is usually asymptomatic. The salient points of clinical diagnosis of bilateral phrenic nerve dysfunction include failure to wean or nocturnal dyspnea, orthopnea and paradoxical abdominal motion during spontaneous breathing in the supine position. Additionally, >50% increase in vital capacity between supine and upright position helps solidify the clinical diagnosis. Ultrasound imaging or diaphragmatic EMGs are the tests of choice for unilateral diaphragm paralysis but they are infrequently pursued due to the lack of therapy and the generally dubious clinical significance. Bilateral diaphragm paralysis is an exceedingly rare complication.
Recovery time for diaphragm dysfunction and paralysis can exceed two years and treatment is aimed at decreasing symptoms of orthopnea and nocturnal dyspnea. This is best accomplished by resting the accessory muscles of respiration at night and preventing hypoxemia during sleep and especially during REM sleep. The diaphragm is the principle muscle of respiration during REM sleep. Mechanical support may consist of prolonged mechanical ventilation via ETT or tracheostomy, BiPAP or CPAP via nasal mask.
Deep vein thrombosis (DVT) and PE are rare complications of cardiac surgery. Clinically suspicious PEs have been diagnosed in 0.5-3% of CABG patients within 2–8 weeks of surgery (JACC.21:990,1993, Ann Thor Surg 53:988,1992). DVT ppx with SQ LMWH or UFH should be started on POD 1 unless there is concern for excessive bleeding or the patient is on full dose anticoagulation for a different indication (Afib, prosthetic valve). Subcutaneous heparin can be started 24 hr post-op in high risk patients and need not be held for chest tube removal or insertion.
Postoperative cardiac surgery patients are maintained with a nasogastric tube (NGT) until extubation. In the rare circumstance that the gastroepiploic artery is used for grafting, patients remain NPO with NGT drainage for 72 hrs in uncomplicated cases. In patients with known severe diabetic gastropathy, it may be appropriate to consider NGT drainage for 24-48 hours since ileus due to the narcotic anesthesia is very common.
One percent of CPB patients develop severe abdominal complications including PUD (47%), Intestinal obstruction or perforation (16%), biliary disease (11%), mesenteric ischemia (11%) and pancreatitis (3%). The mortality from these is 26-59% (A J Surg.167:553,1994, Surg Gyn Obs.165:251,1987).
Stress ulcer prophylaxis is usually begun on POD 1 with Famotidine and is continued until patients are eating well. The diet is resumed when evidence of bowel function has returned. Clear liquids are started and advanced as tolerated. Indications for enteral feeding via duodenal feeding tubes (DFT) in the postoperative cardiac surgical patient is similar to other postoperative patients. Changes in formulation are instituted if diarrhea, constipation or electrolyte abnormalities arise.
Postoperative hyperbilirubinemia is not uncommon in postoperative cardiac surgery patients with perioperative shock or significant blood product requirements postop. CPB, blood transfusion, medications and hepatic venous congestion can raise bilirubin levels in these patients. Asymptomatic hyperbilirubinemia is usually transient requiring observation only. If clinical signs of cholecystitis or pancreatitis arise, further evaluation is warranted.
Postoperative hemostasis remains a problem area in cardiac surgery due to the requirement for extracorporeal circulation to permit surgery. Total hemostatic paralysis is required for CPB followed by complete reversal of the hemostatic state.
The causes of postoperative hemorrhage are listed below:
qualitative/quantitative platelet deficiency
dilution of coagulation factors
inadequate surgical hemostasis
preoperative use of ASA, IIB/IIIA inhibitors
Anticoagulation is administered prior to cannulation in preparation for CPB. The heparin doses used during CPB are in the range of 25,000 to 50,000u. For comparison, the serum heparin levels during CPB are 10x those of a patient with a therapeutic PTT for a DVT. Upon completion of CPB, heparin effects are reversed with protamine. The effects of heparin and the adequacy of protamine reversal are monitored intraoperatively by the activated clotting time (ACT). During CPB, the ACT is in the range of 375-500 seconds. The normal ACT is 90-120 seconds. In the postoperative period, heparin rebound can occur which may lead to increased chest tube output. This can be diagnosed by checking the ACT although it is often managed empirically with an additional 50mg of protamine.
Qualitative and quantitative platelet abnormalities occur during CPB. Platelet interaction with the synthetic surface of the bypass circuit and the blood-air interface alter platelet membrane characteristics and degranulation resulting in a qualitative thrombasthenia. The two major factors resulting in CPB-associated thrombocytopenia are hemodilution and aggregation onto the bypass circuit. In general, platelet function returns after cessation of bypass and the magnitude of platelet dysfunction may be proportional to CPB time.
Fibrinolysis can occur by two major mechanisms. The first is generally milder in nature and is the result of activation of clotting factors during the institution of CPB. This is minimized by the administration of heparin prior to bypass. Anticoagulation to keep the ACT >400 sec has markedly decreased the incidence and severity. The second mechanism is seen in patients who have received thrombolytic therapy. Usually the “lytic state” has abated by the time they arrive to the O.R.; however, the degree of fibrinolysis may exceed the liver’s ability to replete fibrinogen.
Postoperative hypertension can result in serious hemorrhage. Erratic swings in blood pressure or sustained hypertension places undue stress on suture lines and can disrupt established clot in the surgical field. A ruptured bypass graft or aortotomy site can exsanguinate a patient within minutes despite the ability to perform immediate open chest resuscitation.
EVALUATION and TREATMENT
It is important to identify bleeding early and alert the staff surgeon who may have specific concerns relevant to the case. Bleeding occurs ~3% of the time in post op cardiac cases due to the degree of anticoagulation given for these procedures and the extent of potential bleeding sources.
Consider doing a lung US and getting a CXR to assess widening of the mediastinum or increasing pleural effusion if any hemodynamic instability, rising CVP with decreased CI. The attending surgeon must be made aware early in the case of excessive bleeding. Anytime the chest tube output is elevated >2mL/kg/hr with suspicion for bleed the attending should be notified immediately
Check Chest tube drainage
Re-exploration is indicated in the following situations:
- Acute drainage of 500ml in one hour call staff surgeon and plan for a possible trip back to OR unless good reason not to. (Check coag’s)
- Drainage of >400cc/hr X 3 hrs
- Drainage of > 200cc/hr X 6 hrs
(there are always exceptions to these rules)
Assess hemodynamic stability and do not let the MAP drop <60mmHg.
Check coags, give additional protamine, order blood, FFP and platelets
A Thromboelastogram (TEG) would help guide hemostatic therapy, but this lab test is currently unavailable at UHealth Tower
-If coags and platelets are “normal”, but bleeding continues a consumption coagulopathy will ensue and the follow up platelet count will be predictably low and PT high when next checked. You will have to administer blood products to keep up particularly if bleeding rate in excess of 200cc/hr.
-If patient is hypothermic, warming blankets and warming of blood products are a must. With severe bleeding the Rapid Infusion System (RIS), which warms blood products quickly, should be used.
-In a rapidly bleeding patient, a good starting point is to maintain a 1:1:1 ratio of plasma, platelets, red blood cells (JAMA 2015;313:471–82). Consider 1u of PRBC for each 400cc of chest tube drainage. The Hct change will lag behind. Assume also that the chest tube drainage reflects only a portion of the blood loss and don’t forget to give calcium!
Pharmacologic Treatment of Bleeding
Protamine is used to reverse the effects of heparin at a dose of 1 mg per each 100U of heparin given over preceding 3 hrs. After reversal, an activated clotting time (ACT) is checked and the process is repeated if needed. Look in the OR record or ask the anesthesiologist what the last ACT was and how much protamine was subsequently given. In the OR, if the ACT does not respond normally, then a “clinical protamine titration” is performed. This involves the administration of small doses of protamine and plotting the resultant ACTs until a plateau is reached. When ACTs fail to respond, no further protamine is given. In the ICU setting, it would be rare to need more than 50mg of protamine to normalize a “rebound” elevated ACT.
Protamine is not a benign drug, and adverse reactions are well described. There are three types of protamine reactions. Horrow type I reactions present with hypotension and decreased cardiac output. This is often transient and mild in nature. Horrow type II reactions are antibody mediated (IgG/IgE), are more severe and mimic anaphylactoid reactions. Horrow type III reactions are also (IgG/IgE) mediated and are severe. Often termed “catastrophic pulmonary reaction”, this condition is associated with hypotension, severe pulmonary capillary leak syndrome and severe pulmonary hypertension due to thromboxane and C5a release. Severe reactions necessitate discontinuation of further protamine. There is a higher incidence of antibody-mediated protamine reactions in diabetics using neutral protamine Hagedorn (NPH) insulin preparations. This is due to antigen sensitization by the protamine moiety. There is no specific therapy for protamine reactions.
Aminocaproic acid (Amicar) may be used to prevent primary fibrinolysis and inhibit plasminogen activation. Its use intraoperatively is associated with a 40% reduction in bleeding and blood product use. It is administered as a 5 gram IV loading dose and 1 g/hr maintenance (total is generally 10 grams). Possible side effects include hypotension, arrhythmia and catastrophic intravascular thrombosis is given during secondary fibrinolysis (DIC) as well as acute renal failure and mortality (Ann Thorac Surg, 2008). Because of the risk – benefit profile cardiothoracic patients must be considered carefully before receiving Amicar.
Femoral artery sheaths may be present in patients sent emergently to CABG from the cath lab. These should be pulled by a physician/APP once coagulopathy is controlled, typically within the first 12 hours postop. Check a platelet count and PTT. Give 25-50mg protamine if the PTT is prolonged. Consider 6u of platelets if the platelet count is <70k. Direct pressure is held for 30 minutes without releasing pressure. If a large angioplasty sheath, a Femstop device can be used to maintain pressure for a longer period.
Infectious Disease Issues
PROPHYLACTIC ANTIBIOTICS are routinely given prior to incision for valve and coronary artery surgery as well as pacemaker implantation. The CT surgical service gives 1 dose of cefazoline and 1 dose of Vancomycin within 2 hours of starting the cardiac procedure. Only vancomycin is given if pt has a b-lactam allergy.
STERNAL WOUND INFECTIONS occur in approximately 1% of median sternotomy incisions. Risk factors for development of sternal infections and mediastinitis include obesity, diabetes (5x increased risk), bilateral IMA grafting (3.5x increased risk), prolonged bypass time, low cardiac output, reoperation for excessive postoperative bleeding and multiple blood transfusions. Sternal wound infections may present as a suppurative sternal dehiscence, unexplained fever, failure to wean from mechanical ventilation or an asymptomatic unstable sternum. Evaluation of the sternum and retrosternal space is difficult. CT scanning for retrosternal fluid collections and needle aspiration of the retrosternal space to obtain culture material can be performed. Surgical exploration may be required if the preliminary examination is inconclusive.
Valve Replacement Surgery
Mechanical valves are managed with Coumadin beginning on POD 1 or 2 if there are no contraindications. Intravenous heparin is administered after the chest tubes are removed and continued until the INR is 3. No heparin bolus is given to these patients generally. ASA 81mg PO daily should be initiated.
It is often valuable to check the platelet count before heparin therapy since there is a substantial incidence of thrombocytopenia post CPB. The extent of thrombocytopenia may influence your decision to start heparin.
Bioprosthetic valves are managed with coumadin beginning POD 1 or 2 with an INR goal of 2.5 for the first 3 months. These patients are at substantially lower risk or thromboembolism so heparin administration until the INR is therapeutic is not indicated unless another indication exists (e.g. A.Fib). ASA 81mg PO daily should be initiated as well.
The major neurologic problems postoperatively are stroke, brachial plexus injury, and encephalopathy.
Strokes may be evident at the time of emersion from anesthesia or may occur acutely in the first 3-4 days postoperatively. An atheroembolic source is presumed in virtually all cases. There is no data that anticoagulation is of benefit in these patients. Noninvasive evaluation of the carotids is variably pursued depending on their anticipated effect on therapy. Atrial fibrillation may have been detected prior to the CVA but the short duration of these episodes suggests that AF is not in most cases the likely etiology. All patients were intraoperatively monitored with TEE so little is to be gained by repeating the study. Embolic insults originating from atheroma of the aortic arch, loosened by the CBP aortic cannula jet or by aortic cross clamping, are likely key factors given the higher incidence of stroke in older patients and those with protruding atheromata in the aortic arch (J Am Coll Card 20:70,1992). Coronary artery bypass without cardiopulmonary bypass is being used more commonly, particularly in those patients with severe atheromatous disease of the aorta, to attempt to reduce the risk of stroke.
Brachial plexus injury occurs because of excessive sternal retraction, particularly common with the harvest the IMAs, forcing the first rib into the brachial plexus. The typical C8-T1 injury recovers with time.
Encephalopathy in these patients is multifactorial. Patient age is probably the most important factor given that older hospitalized patients are well known to have more CNS dysfunction in response to drugs, the stress of illness and surgery than their younger counterparts. Minimize unnecessary drugs. Remember that paradoxical agitation is common in the elderly given certain benzodiazepines (e.g. lorezepam). With time, the confusion and agitation decreases though it may take several days for some elderly patients to fully recover. Transfer out of the ICU is generally the treatment of choice.
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