Cardiovascular Intensivist Series:  Post Cardiopulmonary Bypass Care

By: Katrina Augustin, MD, RN-BSN

Peer Reviewed: Eric Leiendecker, MD; Lewis McLean, MD

Successful outcomes in these perioperative patients are dependent on optimal postoperative ICU care. “Failure to rescue” these patients from potentially reversible complications in the postoperative period has been linked to significant morbidity and mortality. Hence, it is the cardiovascular intensivist’s job to anticipate and negate these complications when possible.

FIRST, we need to understand not only cardiopulmonary physiology, surgical anatomy, and the surgical procedure, but also the complex pathophysiology that cardiopulmonary bypass (CPB) creates.

The Basics of Cardiopulmonary Bypass (CPB):

CPB provides circulatory support, allowing the heart and lungs to be isolated from the circulation, thus enabling the surgeon to perform surgery on the arrested heart. The key components of a cardiopulmonary bypass circuit consist of the following: cannulas, tubing, reservoir, pump, heat exchanger, and oxygenator. In its most simplified state, venous blood is drained by gravity into the reservoir. A pump than propels it through a heat exchanger and oxygenator before returning it to the arterial circulation. The circuit also contains vents (used to decompress the heart), suckers (suction devices to remove blood from the surgical field), a cardioplegia system for myocardial protection, and hemofilters which can be used for ultrafiltration. CPB, unlike ECMO, contains a reservoir as well as air-blood interface necessitating much higher anticoagulation needs with a typical ACT target of >480. PMID: 28970635

CPB, with its non-pulsatile flow and obligatory exposure of blood to a foreign surface, predisposes to a predictable sequela of derangements affecting multiple organ systems. Most notable of these is a SIRS-like response with capillary leak syndrome and systemic vasodilation as well as multifactorial coagulopathy. These, and many more derangements, will be discussed in detail in this post. Classically the LONGER the CPB time, the GREATER the derangements.

• Standardized handoff with all team members (ICU providers/surgery/anesthesia/nursing/respiratory) is imperative.
• Obtain CXR, EKG, labs including coagulation studies, ABG, lactate, and full set of pulmonary artery catheter (PAC) numbers (hemodynamics)
• CXR: ascertain the correct position of ET tube, PAC, CVCs, and drains. Ensure no hemothorax or pneumothorax
• Labs: intervene on coagulopathy, electrolyte derangements, etc.

Now, post-CPB pathophysiology and treatments by organ system…

CPB derangements:

• The combination of a non-pulsatile low flow state with significant hemodynamic derangements, cross clamping of aorta with risk of atheroembolism, aortic cannulation with risk of dissection, risk of watershed infarcts especially in those with carotid/vertebral stenosis, inflammatory and neurohormonal derangements, risk of air embolization, and even micro emboli from the CPB circuit all predispose to neurological injury. Neurological insults can range from acute ischemic and hemorrhagic CVAs with significant morbidity and mortality to “postoperative cognitive dysfunction or decline”, postoperative delirium, and seizures. PMID: 8948560

• Treatment
  • Reverse neuromuscular blockade (be sure nearing normothermia)
  • Wake them up and get a neuro exam ASAP. Stop, or minimize sedation, while ensuring adequate pain control
  • If need to reinitiate sedation prioritize short-acting agents (propofol) or consider dexmedetomidine to help facilitate earlier extubation. Both agents can cause hypotension and dexmedetomidine can also cause significant bradycardia
  • If open chest typically requires deep sedation after brief SAT

• Pain: important to optimize for not only patient satisfaction but also to prevent delirium and optimize pulmonary function and regaining of functional residual capacity (FRC)
  • Multimodal analgesia including APAP, opioids (initial IV with transition to PO when able), pain dose ketamine, regional anesthesia (pecto-intercostal fascial plane block, other fascial plane blocks, or epidurals). Incorporation of blocks while minimizing opioids can aid in meeting Enhanced Recovery After Cardiac Surgery (ERACS) guidelines and optimizing outcomes. PMID: 30412813

• • If no renal dysfunction, can consider Toradol as a great opioid sparing agent. Despite black box warning after CABG in 2005, more recent data supports its safety and efficacy PMID: 24231193, PMID: 32393370

• Hypothermia: many cases will be done under normothermic CPB (temp >34C); however, there is still significant heat loss from pericardial irrigation, open body cavities, and administration of large quantities of crystalloid/blood. Hypothermia predisposes to arrhythmias, vasoconstriction (with decreased CO), coagulopathy, insulin resistance, and delayed extubation.
  • Rewarm, passively vs. Bair hugger
  • Beware rewarming frequently causes vasodilation with increased venous capacitance and subsequent hypotension that may need to be combatted with a vasopressor or additional volume resuscitation

• Postoperative delirium (PMID 29621031): high risk due to significant operation with neuroinflammation + immobility from IABPs, femoral Impella CP, and sheaths limiting mobility
  • Incidence 14-50%, higher risk if older, previous neurocognitive dysfunction, etc.
  • All the normal stuff–>ABCDEF Bundle: treat pain, early extubation, avoid deliriogenic meds, early ambulation, DC tubes/lines when no longer needed

CPB derangements: Despite cardioplegia, and the best attempts at cardioprotection, the heart rarely escapes unscathed.

Some key concepts before diving in… 

• Hemodynamic lability is often the “norm” in the immediate post-op period

• Always keep a broad Shock Differential post-operatively
  • Cardiogenic: myocardial stunning post CPB, MI and graft failure, acute valvular dysfunction, RV failure, arrhythmia/CHB (electrical etiology), hypocalcemia
  • Hypovolemic/hemorrhagic: acute blood loss, massive diuresis
  • Distributive: excessive sedation, vasoplegia /SIRS-like response, anaphylaxis, (VERY unlikely  to be infection/sepsis unless pre-existing)
  • Obstructive: tamponade, LVOT obstruction, PE, tension PTX
  • Neurogenic: neurogenic with spinal cord infarction due to ischemia or embolic phenomena

• Typically, lactate will peak in the early post-operative period as the patient is resuscitated/warmed and lactate is flushed from previously vasoconstricted vascular beds. Imperative to interpret this in the context of patient hemodynamics, vasopressor requirements, and other clinical data/laboratory results to determine if it is the normal course or instead worsening shock.

• Trajectory: As reperfusion and inflammatory response from CPB/ surgery subsides most patients with uncomplicated course (rapid recovery/”fast track” patients) can be weaned off inotropic therapy/vasoactive medications in the first 6-12 hours of their ICU stay.

• Low cardiac output syndrome (LCOS) after cardiac surgery, characterized by inadequate cardiac pump function with impaired DO2, is a not infrequent (incidence 2-27%) complication after cardiac surgery and ranges from mild myocardial stunning to severe cardiogenic shock (CS). Imperative for the intensivist to constantly be monitoring for this. PMID: 36247457

• Typically MAP goals between 60-90/SBP 90-140
• May need higher MAPS in pts with history of HTN, RV dysfunction, renal insufficiency
• Lower MAPS in pts with LV dysfunction, mitral valve repair, regurgitant lesions, active bleeding, or vulnerable aortic suture lines

• Inotropic and lusotropic effects

  • CPB effects
    • Ischemia reperfusion injury is common with decreased ventricular compliance/diastolic dysfunction and transient myocardial stunning. Further complicating this is risk of coronary air embolism (most commonly RCA) and iatrogenic coronary injury (Mitral valve–>circumflex, Tricuspid valve–>RCA, aortic root replacement–>obstruction of a coronary button) further contributing to regional myocardial dysfunction. Tissue edema/wiring of the ribs decreasing chest wall compliance can further impair myocardial diastolic function impairing filling and CO.
    • Myocardial stunning nadir is variable but typically in the first 4-12 hours post-op. Pts with pre-existing low LV EF/ RV dysfunction are at higher risk

• Treatment
  • Straightforward pts (minimal inotropic support and rapid normalization of cardiac function) can typically have a rapid inotrope wean based off hemodynamics in the immediate post-op period (first 6-12 hours arriving to ICU)
  • Higher-risk patients with significantly decreased cardiac function typically benefit from much slower inotrope wean often over 24 hours or even days; rapid weans can lead to decompensation, worsening CS, and even need for MCS
  • INOTROPES are a data light zone (DoReMI, 37649849  36268289) with existing RCTs not demonstrating significant differences in outcomes between agents thus leading to tremendous practice variability amongst providers/institutions. Studies looking at epinephrine typically have significant confounding with epinephrine added as last line agent and/or in patients on higher vasopressor equivalents. Recent cardiac shock paradigms suggest severe CS is often associated with a systemic inflammatory response which can cause low SVR and potentiate hypotension and thus it could induce significant confounding if the groups placed on epinephrine (inopressors) are sicker than those just requiring inodilator therapy alone to optimize coronary perfusion pressure and end organ perfusion. PMID: 23977106

• Typical agents in the U.S.
  • Inodilators: milrinone/dobutamine
  • Inopressor: low dose epinephrine (my dosing 0.01 mcg/kg/min-0.08 mcg/kg/min), norepinephrine, and high-dose dopamine

• My Practice pattern (data free!!!)
  • Choose my inotrope tailored to individual needs
    • SVR (high or low)
    • PVR (milrinone more effective at decreasing PVR)
    • Chronotropy (I tend to see more tachycardia with dobutamine)
    • Lusitropy (pts with significant decreased compliance/LVH may benefit from milrinone)
    • Kidney function (may still use milrinone but err towards lower doses and monitor closely for hypotension)
    • Onset (epi/dobutamine quicker onset)
    • RV failure (milrinone may seem great due to decreased PVR but only use if you can do without causing hypotension. Hypotension in RV failure can cause rapid deterioration)

• Big Picture: Inotropes increase myocardial demand, are arrhythmogenic, and should be used judiciously to optimize end organ perfusion. Escalating levels of inotropes should call for consideration for mechanical circulatory support (MCS)
• Delayed chest closure can also be helpful in some pts to optimize CO and increased diastolic filling that can be impaired by “tight mediastinal syndrome” PMID: 37131284

• Afterload

  • CPB effects
    • Decreased afterload: Multifactorial 2/2 exposure of blood to non-endothelialized CPB surface with subsequent SIRS like response with vasodilation. Pre-operative medications such as ACE-inhibitors, milrinone, and relative ADH deficiency can also contribute to significant vasoplegia. Especially common in long bypass runs with cumulative risk in some situations (such as low LVEF, or blood product use).
    • Increased afterload: not uncommon, multifactorial due to hypothermia-induced vasoconstriction, pain/inadequate sedation, peri-op cessation of home antihypertensives, and injudicious vasopressor use. Increased afterload causes decreased CO (earlier AV closure and decreased SV), potentiates bleeding, and can threaten fragile anastomotic sites
    • To make it more complicated can have increased afterload and simultaneous hypotension–> increased afterload contributing to low CO and hypotension.

• • RV afterload can be significantly increased due to Protamine induced thromboxane A2 release, CPB induced increased endothelin-1 levels and Hypoxia/hypercarbia/acidosis
  • Remember BP/MAP is labile in post-op period. One study noted 90% of patients needed medications to decrease BP at least once perioperatively PMID: 10890479. Increased MAP does NOT EQUAL increased CO or oxygen delivery, in fact it can cause decreased SV (if elevated SVR) and systemic hypoperfusion with resultant ischemia

• Treatment
  • Hemodynamic State: Decreased afterload + hypotension+ adequate CO (pure vasoplegia)
    • Norepinephrine/vasopressin
    • Typically avoid phenylephrine (unless dynamic LVOT obstruction) as it can decrease bypass graft flow/worsen pHTN, etc
    • Hydroxocobalamin or methylene blue (avoid with serotonergic meds/G6PD/pHTN)
    • Angiotensin as last resort- should be a very rare occasion its needed
  • Hemodynamic State: Increased afterload + hypertension + normal or low CO
    • Vasodilators therapy will decrease afterload with resultant increase in SV/CO (inotrope is not always the answer for low CO); vasodilators can also decrease risk of arterial graft vasospasm
    • Frequently this phenotype is seen in pts who are hypovolemic post bypass and thus have decreased preload with low CO compensated by elevated SVR (Forrester classification “cold and dry) and may just need volume resuscitation
    • Short acting agents preferred: Clevidipine/nitroglycerine (or sodium nitroprusside-less likely in U.S). Can consider nicardipine but longer half-life and less forgiving for dynamic hemodynamics with risk of sudden deterioration
    • If decreased EF/RV dysfunction milrinone can be effective for afterload reduction + increased inotropy
  • Hemodynamic State: Increased afterload+ low CO causing hypotension
    • Typically benefit from inodilator (milrinone/dobutamine) +/-norepinephrine. Low threshold to consider mechanical circulatory support in these patients if they are deteriorating

• RV failure due to increased RV afterload
  • Inhaled pulmonary vasodilator therapy (iNO/epoprostenol)
  • Avoid hypoxia, hypercarbia, and acidosis
  • Can consider milrinone to decrease PVR/RV afterload; however, ensure adequate RV perfusion/MAP first as milrinone can cause hypotension which is NOT tolerated in RV failure. Vasopressin great vasopressor in RV failure (increases SVR but not PVR) but can use norepi/epi as well

• Beware refractory hypotension despite escalating vasopressors/inotropes as it may be a dynamic LVOT obstruction
  • TTE with dynamic underfilled LV, intracavitary gradient (>30 mmHg), eccentric MR due to combination of drag forces + venturi effect (suction) on the anterior MV leaflet with systolic anterior mitral valve motion (SAM)
  • Classically seen with hypertrophied LV (especially eccentric septal hypertrophy), post aortic or mitral surgery (with steep aorto-mitral angle increasing risk), low afterload state, volume depletion, high catecholamine state. Secondary dynamic LVOT obstruction can also occur due to severe RV dysfunction causing decreased LV preload in a hypertrophied ventricle.

• Preload

  • CPB effects
    • Decreased preload 2/2 increased venous capacitance (SIRS-like response/rewarming), third spacing (increased capillary permeability due to CPB-induced inflammation), acute blood loss, cardiac ischemia-reperfusion injury with decreased ventricular compliance requiring higher filling pressures, aggressive intra-operative hemofiltration, and cold diuresis
    • Increased preload: may be seen with significant intra-op coagulopathy requiring massive transfusion protocol or excessive crystalloid/colloid resuscitation

• Treatment
  • Attention to volume resuscitation is CRITICAL in the post-op period. Amount is highly variable, but unusual to need more than 2-3L of crystalloid
  • Volume responsiveness:
  • Trends in CVP/ PA diastolic pressure/PCWP are frequently used as surrogates of preload in this population. As always there are limitations with static markers; however, some data suggests there may be increased utility of PAC pressures in this population PMID: 21352541

• Dynamic measures are likely superior
  • Fluid bolus with pre and post cardiac index
  • Passive leg raise
  • One study found change in pulse pressure after 15 sec expiratory hold was most sensitive/specific in this population (deranged physiology)
  • Many of the dynamic measures typically used are very limited in this population
• When interpreting PA catheter numbers remember PRESSURE DOES NOT EQUAL VOLUME
• Pts with left ventricular hypertrophy (LVH), or long cross-clamp times with significant ischemia reperfusion injury, often have impaired LV compliance/diastolic dysfunction causing an upward and leftward shift of their PV loop where for a set PCWP (LVEDP) they will actually have a lower volume status than expected (i.e. Despite a PCWP of 15 they may still be underfilled requiring more volume) PMID: 18835782

Image: Source: Anesthesia Key; Depicting PV loop with diastolic dysfunction/decreased compliance with leftward/upward shift of EDPVR with resultant increased LVEDP at a lower LVEDV when compared to normal PV loop

• What fluid? Crystalloid vs colloid?

• • Although it seems like the CV ICU runs on albumin at times, there is no data that it, or any specific fluid, is superior PMID: 35852528
  • Important to avoid volume overload which can cause pulmonary edema, hemodilution with increased transfusion requirements, intestinal dysfunction, and increased hospital LOS
  • If needing excessive volume be sure to R/O other causes of hemodynamic instability.
  • Echocardiography is essential to build a complete hemodynamic picture. TEE can be your best friend as TTE may have very limited views in the early post-op period

• Chronotropy/Rhythm

  • CPB effects
    • Bradycardia common. Multifactorial due to anti-tachyarrhythmia prophylaxis (B-blockers/amio), direct trauma to conductive tissue especially during valvular surgery, myocardial/nodal tissue edema, and electrolyte derangements. Can see SB, junctional/idioventricular rhythms, atrioventricular conduction delays, CHB, and even asystole.

• • • Post-operative atrial fibrillation (POAF), common (IncidenceCABG 20-30%, valve surgery 35-40%, CABG +valve as high as 60%); multifactorial due to systemic & pericardial inflammation, adrenergic stimulation, metabolic derangements, volume overload, and direct cardiac manipulation. Loss of atrial contraction associated with up to 30% decrease in CO, may not be tolerated especially in pts with significant LVH/diastolic dysfunction/RV failure (PMID: 28369234)

• • • Ventricular arrhythmias are uncommon. Should raise suspicion for ongoing ischemia (grafts down, coronary button occlusion on aortic root replacements) PMID: 24511410

• Treatment
  • Bradycardia/conduction abnormalities
    • Temporary epicardial atrial & ventricular pacing wires typically placed intra-operatively if any concern
    • Atrial pacing preferred to optimize CO (AAI) if AV conduction intact
    • Sequential atrial-ventricular pacing if AV conduction impaired (DDD)
    • Ventricular pacing (VVI) should only be use as backup/rescue. Though may need to be used if no atrial wires placed or atrial wires no longer functional (always seem to stop working first) PMID: 25962078
    • Pacing thresholds need to be checked ideally q shift; important to identify changing thresholds especially in those that are pacer-dependent
  • AV block >7 days typically indication for pacemaker. Risk of pacemaker varies depending on operation (6.6% AVR, 10.5% MVR, 13.3% AVR+MVR, CABG<1%) PMID: 31753204
    • Chronotropic agents such as isoproterenol/epi/dopamine can be used for chronotropy but increased myocardial work/arrhythmias so not ideal
    • Can manipulate HR to optimize CO (HR x SV= CO), though in pts with significant diastolic dysfunction can impair diastolic filling time so caution recommended
  • POAF prophylaxis (PMID: 28369234):
    • B-blockers first line if not requiring vasoactive therapy; use often limited due to c/f adverse effects (negative inotropy/chronotropy/hypotension); most useful in rapid recovery patients
    • Antiarrhythmics, most commonly amiodarone (less negative inotropy than BB in hemodynamically unstable pts)
    • Magnesium, atrial pacing
  • POAF management (PMID: 28369234, PMID: 35649561):
    • Rate or rhythm control appropriate in hemodynamically stable asymptomatic a-fib per AHA guidelines
    • Cardioversion for hemodynamic instability
    • NO AC for POAF <48 hrs duration; greater than 48hr duration needs to weigh individual risk factors for post-op bleeding vs prevention of thrombotic events (expert opinion rec minimum of 4-6 weeks AC)
    • IMPORTANT TO HAVE CLOSE LONG TERM FOLLOW-UP as they are higher risk for CVA/thrombotic events and have increased mortality
  • Ventricular arrhythmias management
    • Antiarrhythmics (amiodarone/lidocaine/ibutilide)
    • Cardioversion/defibrillation
    • Stellate ganglion block
    • Low threshold for cath lab for assessment of grafts/coronary button occlusion
    • Mechanical circulatory support for refractory arrhythmias

CPB derangements (deranged physiology):

• Post-operative hypoxia
  • Mechanical etiologies
    • PTX->may need to be addressed if there was inadvertent opening of pleural space with no chest tube
    • ET tube migration
    • Mucous plugging
    • Phrenic nerve injury (direct trauma/retraction injury/cold slushy/IJ hematoma from cannulation) typically causes more ventilation issues than hypoxia
  • Pulmonary edema
    • SIRS-like syndrome with capillary leak
    • Reperfusion injury to lungs especially if prolonged CPB
    • Volume overload especially if coagulopathy with MTP
    • Poor LV function
    • Inadequate LV venting
  • Intra-pulmonary shunt
    • Incomplete lung reinflation with atelectasis-typically lingula/LLL
    • Pleural effusions (if so check CTs to be sure draining)
    • Decreased chest wall compliance (sternum wired)
    • Vasodilator (nitroglycerine/clevidipine) inhibition of hypoxic pulmonary vasoconstriction
  • Intracardiac shunt
    • 10% of population have patent foramen ovale, post CPB induced pHTN can lead to increased right sided pressures with new R->L shunt

Management:

• Despite the scary list above, many patients with uncomplicated case do well and can be extubated within 6 hrs of ICU arrival per ERAS guidelines.
• Having a nurse/respiratory therapist driven protocol for extubation on patients that meet specific criteria can facilitate better adherence with ERAS goals of early extubation
• Minimizing sedation also helps
  • My checklist:
    • Are they warm?
    • Awake and able to protect their airway
    • Stable trajectory (not on increasing doses of inotropes/vasopressors or requiring extensive resuscitation) with no need for RTOR
    • Adequate lung mechanics
    • Not too dependent on PEEP. Yes, NIV may be a great option, but use care with …
      • Volume overload with congested lungs and hypoxia
      • Myocardial stunning with severe LV dysfunction->remember extubation will increase their preload and afterload
    • The Not so straight forward cases
      • Lung protective ventilation, especially if they develop ARDS
      • PEEP titration to optimize functional residual capacity (FRC) PMID: 29763183
      • Adequate analgesia to optimize lung mechanics
      • Early mobilization to help with regaining FRC
    • The RV failure patient
      • PEEP titration to FRC to optimize PVR (preventing under-recruitment/atelectasis as well as overdistention/barotrauma) PMID: 29763183

Figure: Source deranged physiology; FRC=point where lung elastic recoil and the chest wall outward expansion are balanced and equal. i.e. the lungs are optimally opened with lowest PVR and best ventilation/oxygenation

• Avoid hypoxia (may target a higher PaO2 85-100), hypercarbia, and hypercapnia PMID: 25962078
• Consider inhaled pulmonary vasodilator (iNO/epoprostenol)

• CPB derangements (PMID: 34945041):

• • Arterial hypotension, non-pulsatile flow, low CO, hypovolemia, anemia, hemolysis, ischemia-reperfusion injury, and venous congestion can all contribute to cardiac surgery associated-acute kidney injury (CSA-AKI). Higher risk of CSA-AKI with more complex operations requiring longer CPB time/aortic cross clamp time as well as need to go back onto CPB after initial separation.

• • Staged same as other AKI via KDIGO staging (stage 1 (1.5-1.9 x baseline) 2 (2-2.9 x baseline), 3 (3 x baseline or >4 mg/dl or initiation of RRT)

• • • NEW and FUN: new biomarkers involved in tubular ischemia/cell cycle arrest that can predict progression to AKI after cardiac surgery are now FDA approved (Nephrocheck). Attempts at minimizing CSA-AKI are typically focused on avoidance of peri-operative/intra-operative hypotension, venous congestion, and hypoperfusion

• • May have initial cold diuresis/polyuria in some patients especially if they received mannitol intra-op (sometimes used as a free radical scavenger). Replace electrolytes especially K+/Mg to avoid arrhythmias. If excessive polyuria may require significant volume replacement

• • Acidosis–>no matter how fabulous our colleagues in the OR resuscitate typically there is a component of metabolic acidosis. Often lactate peaks in ICU (potentially flushed from previously constricted beds vs epinephrine use (type B lactate) vs need for ongoing resuscitation.

• • Always ask yourself is the elevated lactate due to decreased DO2 or Not?
    • If yes, may need volume/inotropes, blood, or even MCS dictated by hemodynamics/labs.
    • If No, maybe just needs time and a calm intensivist:)
  • Severe acidosis can predispose to arrythmias/ increased RV afterload, and depressed myocardial function. Animal data suggests this is not a problem till pH <7.1-7.2. As a whole cardiac ICU seems to culturally err towards bicarb sooner than non-CV ICUs despite not great data. If using Bicarb, beware of hypernatremia, rebound alkalosis, and many other side effects. PMID: 25962078   THAM solution (an organic amine buffer that works as a proton acceptor) is a great alternative base to bicarb and does not cause a respiratory acidosis and hypertonicity that bicarb does.

• • Volume Status
    • Typically, most adequately resuscitated patients will be anywhere between 3-6 L positive over the first Post-op day PMID: 25962078
    • As the inflammatory response subsides/myocardium recovers, extravascular fluid is reclaimed through the lymphatics, and hypervolemia typically ensues by POD 2 (variable) requiring de-resuscitation

• • Timely de-resuscitation is imperative
    • Too early: can cause hemodynamic destabilization and renal injury if intravascularly deplete despite whole body volume overload. May be more likely in pts with ongoing vasoplegia and increased venous capacitance and third spacing
    • Too late: can lead to venous congestion and risk of organ dysfunction including AKI
    • RV failure: may warrant earlier volume removal to optimize CO (remember RV volume overload can cause decreased LV preload and thus CO due to intraventricular dependence); if unresponsive to diuretics may require RRT in some cases
    • Nuances in volume management come into play with specific conditions. For example, a hypertrophied LV predisposed to dynamic LVOT obstruction may benefit from later and/or more judicious volume removal while other conditions such as dilated cardiomyopathy with MV dysfunction may benefit from earlier volume removal.
    • Some centers do less volume expansion/more ultrafiltration with lower net positive states while others may tend to resuscitate more heavily which can also contribute to timing and degree of de-resuscitation required

CPB derangements: Risk of mesenteric ischemia, bleeding, ileus, hepatic dysfunction, and pancreatitis in setting of low flow, thromboembolic events, and venous congestion. PMID: 25208431

• If an uneventful case, goal for extubation, swallow evaluation and CLD subsequently advanced to goal as tolerated.
• If aortic total arch repair-> assess for recurrent laryngeal nerve injury
• Patients with high dose vasopressors and low flow states are higher risk for mesenteric ischemia so always be suspicious of an elevated lactate that is unexplained-low threshold for CT imaging or flexible sigmoidoscopy
• Early bowel regimen in the setting of post-op opioids

CPB derangements PMID: 25962078, PMID: 33251719:

• Coagulopathy from CPB is multifactorial with a tendency to bleed and clot!
  • Exposure of blood to the foreign surface of CPB leads to widespread activation of the coagulation system and inflammatory systems. Inflammatory cytokines cause further upregulation of the coagulation system with resultant depletion of coagulation factors, hyperfibrinolysis/hypofibrinogenemia, and quantitative and qualitative platelet disorders.
  • Hemodilution from circuit priming + crystalloid resuscitation, acute blood loss, hypothermia, and the requirement for high dose heparin due to the thrombogenic nature of CPB further contribute to coagulopathy. Antiplatelet agents onboard may not be helping either!
• TXA (shown to decrease post-operative bleeding/transfusion requirements in pts post cardiac bypass) typically initiated in the OR at end of case and infusing for several hours in ICU. High dose TXA associated with increased risk of seizures PMID: 27774838, PMID: 31307381

• Definitions of excessive bleeding are variable. Rough guide to concerning CT output is >400 1^st hour, >300 for first 2hrs, > 200 for 3 consecutive hours. Potentially more concerning is sudden INCREASE in bleeding or sudden DECREASE in bleeding (accumulating hemopericardium/hemothorax)

• Treatment of the bleeding patient
  • First, warm the patient
  • Get a full set of coags, including K-TEG and H-TEG (if concern for residual heparin effect- or heparin rebound) as well as calcium
  • Correct coagulopathy (FFP, protamine, cryoprecipitate, platelets/DDAVP, pRBCs) and replace calcium
  • If warm patient with no evidence of coagulopathy (no medical etiology for bleeding) than it may be surgical and require RTOR. Call your surgical colleagues EARLY

• Expect thrombocytopenia, classically platelet count decreases by 50%, with nadir 48-72 hrs post-surgery. So, hold on sending those HIT panels 🙂 PMID: 31816284

• Hgb/Hct transfusion thresholds in cardiac surgery remain controversial. Studies with mixed results
  • “Transfusion Requirements After Cardiac Surgery trial” targeted hct 24% vs 30% with no difference in mortality/major morbidity and showed significant decrease in transfusion requirements in restrictive group
  • Transfusion Indication Threshold Reduction trial targeted transfusion with hgb <7.5 vs < 9 found no difference in primary composite outcome (serious infection + ischemic event at 3 months) but did note a significant secondary outcome of increased 90 day mortality in the restrictive group
  • TRICS trial: noninferiority between transfusion thresholds in cardiac surgery patients at a Hgb of <7.5 vs <8.5 g/dL
  • Importance to balance risks of transfusion (TRALI/TACO/sensitization, etc) with benefits.

• Typically, ASA within 6 hours post CABG with controlled CT output PMID: 25679302

Do all the standard critical care things except for DVT prophylaxis.

• Timing of DVT prophy variable based on patient bleeding risk, surgeon preference, and patient’s other indications for anticoagulation; best made with shared decision making with our surgical colleagues

PAC: Line should curve without loops or knots into the main PA, with the distal tip in right or left PA (about 3-5 cm from midline), typically ending within hilum. ENSURE IT IS NOT INADVERTENTLY WEDGED. Know your waveforms cold!

            Figure: PAC ending in right PA (hilum region on X-ray)

Figure: PAC with CVP and PA waveform. Important to recognize PA waveform from PCWP and RV waveform to ensure catheter has not migrated

Source: RK. MD. https://rk.md/2017/pulmonary-artery-catheter-structure-waveforms/

• PAC hemodynamics should be measured at end expiration after having transducer leveled at phlebostatic axis and lines zeroed.
• Thermodilution: Injection of cold (or room temp) fluid in proximal PAC port causes cooling of blood with the change in temperature noted by the thermal sensor in the PA; the faster flow (greater CO) leads to a more rapid change in temperature (cold quicker, followed by rewarming faster) with smaller AUC
  • Limitations of thermodilution: anything that alters typical direction of cardiac flow (leads to cold blood mixing with warm blood and alters the change in temperature measured at the thermistor). Examples: severe TR/PR, ECMO (PMID: 34860710), and potentially ASD/VSD. Inadequate technique (slow injection, incorrect injectate volume, etc) can also cause it to be inaccurate
• Indirect Fick: Requires PA sat (ideally) and simultaneous arterial saturation; divides estimated O2 consumption (125 ml/min/m2) by difference between arterial and venous O2 content to obtain CO.
  • Limitation: Assuming a fixed O2 consumption can introduce error but following trends in Fick CO can often still be helpful
  • Direct FICK: gold standard where actual O2 consumption is measured using Douglas bag/indirect calorimetry; typically, not done clinically due to complexity

IABP (one of the few times a DAILY X-RAY indicated): Goal: IABP tip radiopaque marker distal to left subclavian artery origin with termination of balloon above splanchnic vessels.

• Target 1-2 cm below aortic knob but at or above level of the carina, one study recommending 2 cm above carina as ideal PMID: 17717232

Figure: A) IABP appropriately placed B) IABP inappropriately low (well below aortic knob and sitting below carina) placing patient at risk for mesenteric ischemia with low riding balloon

Impella (placement confirmed on echo/bedside cardiac US): 

• Impella 5.5: approximately 5-5.5 cm from AV annulus (bend at annulus) to the mid-inlet of inflow cage on parasternal long axis view; ensure inlet is not abutting MV apparatus
• Impella CP: inlet of catheter (not pigtail) approximately 3.5 cm below AV annulus

Figure: Impella 5.5 on parasternal long axis view with appropriate placement

ECMO cannulas:

• Venovenous (VV) ECMO (*needs photo of VV configurations)
  • Femoral-IJ configuration: femoral drainage junction of RA-IVC, be sure tip not in hepatic veins; to prevent recirculation typically maintain IJ return cannula at approx. 8-10 cm separation from drainage cannula tip
  • Fem-fem cannula placement nuanced/variable. My preference(for fem-fem) is right CFV bicaval multistage drain with a left CFV single stage return positioned in the right atrium to minimize re-circulation
  • Bicaval dual lumen cannula (Crescent): Typically RIJ or left subclavian to allow appropriate positioning of return flow directed across tricuspid valve, radiopaque markers for SVC/IVC drainage as well as catheter tip (seated well into IVC), and radiopaque marker for return to allow flow directed towards tricuspid valve. Flow across the tricuspid valve can be confirmed on echo
  • ProtekDuo RVAD: Typically placed via RIJ, distal tip in main PA

Figure: A) Femoral- IJ configuration with 10 cm of separation; B) Fem-Fem configuration with attempt for bicaval drainage (likely should be several cm higher) with return cannula positioned in right atrium (Photo B: credit to Lewis McLean)

• Venoarterial (peripheral): multistage femoral venous drainage typically bicaval with distal tip in SVC to optimize drainage; common femoral arterial cannulas are short typically distal tip in iliac artery on KUB

Figure: A) multistage drainage cannula with tip in SVC allowing for bicaval drainage; B) Arterial cannula with distal tip in Iliac artery on KUB

Chest tubes: Goal to discontinue as soon as drainage acceptably low as it minimizes patient’s pain (they really HURT) but realistically in the CVICU it is the surgeon that says when they come out.

Foley catheter, CVCs, and ET tube per norm management

Take Home Points

• Successful outcomes in these perioperative patients are dependent on optimal postoperative ICU care

• Vigalence and equanimity are needed to prevent overreaction to self limited hemodynamic swings while simultaneously recognizing and intervening on concerning trends

• CPB predisposes to a predictable sequela of derangements affecting multiple organ systems; most notably a SIRS-like response with capillary leak syndrome/systemic vasodilation as well as multifactorial coagulopathy

• These patients will require INITIAL resuscitation followed by TIMELY de-resuscitation

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Katrina Augustin

Cardiovascular Intensivist and emergency Medicine Consultant at Mayo Clinic, Rochester, MN Campus

Katrina (Trina) Augustin is a Cardiovascular Intensivist and Emergency Medicine consultant at Mayo Clinic in Rochester Minnesota where she also works as part of the ECMO team. She completed an Emergency Medicine Residency and chief residency at the University of Pittsburgh Medical Center. Trina's interests include cardiovascular critical care with a focus on mechanical circulatory support devices including ECMO. She is passionate about using FOAMed as an educational opportunity to improve the care of patients presenting with cardiovascular emergencies.

Latest posts by Katrina Augustin (see all)

• CV-EMCrit – MCS Minute Series: Differential Gas Exchange on Peripheral Femoral VA ECMO with Trina - September 16, 2024
• CV-EMCrit – Cardiovascular Intensivist Series:Post Cardiopulmonary Bypass Care (CABG) with Trina Augustin - May 25, 2024
• CV-EMCrit Wee – MCS Minute: ECMO and the DO2/VO2 ratio with Trina Augustin - January 31, 2024