Postoperative cardiac surgical patients

general postoperative management
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initial evaluation in ICU

Chest tube output.
ECG.
Chest radiograph.
Pressor requirement.
Labs:
- ABG/VBG.
- Electrolytes including iCa/Mg/Phos.
- Lactate.
- Complete blood count.
- INR, PTT.
- TEG.
- Anti-Xa level.
- Fibrinogen level.
Ventilator mode is ASV mode on arrival to ICU:
- Follow minute ventilation, saturation, and etCO2.
Examination, focusing on:
- Skin perfusion (temperature, mottling, capillary refill).
- POCUS (cardiac views if possible; femoral vein Doppler).

general postoperative objectives

Weaning off pressors/inotropes as able (especially after >6-12 hours).
Extubation (target extubation within <6 hours for ERAS patients if other objectives are met).
Multimodal analgesia (discussed below ⚡️)
AF prophylaxis: ⚡️
- Magnesium sulfate 2 grams IV daily as slow infusion; follow Mg level targeting >>2 mg/dL.
- Amiodarone 400 mg PO BID.
- Metoprolol 12.5-50 mg PO BID starting POD #1 if possible.
GI prophylaxis: 40 mg PPI daily (note: greater efficacy & lower delirium risk than H2RA).
Antiplatelet & anticoagulant strategy:
- Varies depending on the procedure; discuss with surgeon.
- DVT prophylaxis may often be started POD #1.
Consider gentle diuresis once hemodynamics are stably recovering (e.g., POD1).

postoperative chest radiograph
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ETT 📖

Ideal height above carina depends on head position (judged by the position of the mandibles):
- Neutral position: ideally 5 cm +/- 1-2 cm above the carina. (Shepard 2019; 36832087; 22391269)
- Neck flexion: ideally ~2-5 cm above the carina.
- Neck extension: ideally, perhaps ~5-8 cm above the carina.
ETT should be located around the depth of the aortic knob.

IABP 📖

~2 cm below the superior aspect of the aortic arch. (Shepard 2019)
Slightly above the left main bronchus.

right heart catheter

The ideal position is within the right or left main pulmonary artery or within the proximal interlobar pulmonary arteries (within <1-2 cm of the lateral edge of the mediastinum).
As a general rule of thumb, if the catheter extends beyond the hilum of the lung, it should be retracted. (22013292)

epicardial pacing leads

mediastinal drains

mediastinal width

Follow the distance between the mediastinal silhouette and the SVC (based on the location of a right heart catheter) and/or pacer wires.
Widening mediastinum may suggest undrained blood is accumulating. (Bojar 2021)

postoperative concerns after SAVR
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**impaired diastolic function (e.g., normal EF with a small chamber)**

This commonly occurs in the context of surgical AVR.
Maintain sinus rhythm with AV synchrony, if possible.
The optimal heart rate may be ~80-90 b/m. (Bojar 2021)
Fluid resuscitation to target a somewhat elevated LV filling pressure may be helpful (e.g., PAD ~20-25 mm). (Bojar 2021)

paravalvular leak

Consequences of a paravalvular leak may include hemolysis and heart failure.
Management may include reoperation or percutaneous closure devices.

LV outflow tract obstruction (LVOTO)

May result from LV hypertrophy, following relief from elevated afterload.

postoperative concerns after TAVR
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heart block

Timing: Onset can be delayed for some days after the procedure as the prosthetic valve expands, causing traction on the cardiac conduction system.
Risk factors:
- Bundle branch block at baseline.
- Large left atrial size.
- Type of TAVR:
  - Original Edwards Sapien valve: 1.8-8.5% risk.
  - Sapien 3: up to 10% risk.
  - Medtronic Core Valve: 20-40% risk. (Flynn 2020)
Management guidelines: (31439219)
- Indications to leave a transvenous wire in overnight:
  - New LBBB.
  - Persistent increase of >20 ms in the PR or QRS duration with a preceding conduction disturbance (RBBB, LBBB, IVCD, or 1st-degree AV block).
- Indications to consider ongoing monitoring:
  - Persistence of worsened conduction (as listed above).
  - PR >240 ms.
  - QRS >150 ms.
- Indications for insertion of a permanent pacemaker:
  - High-graade AV block.
  - 3rd degree heart block.

acute hemodynamic deterioration

differential diagnosis

Hemorrhage.
Arrhythmia.
Tamponade.
Paravalvular leak:
- Typically diagnosed intraoperatively via echocardiography.
- Less likely with newer TAVR designs.
- Treatment may require surgical intervention or valve re-expansion.
MI:
- Rarely, the valve may overlie the coronary ostia.
- Risk is increased with valve-in-valve procedures. (Flynn 2020)
Mitral valve apparatus injury.
Dynamic LV outflow tract obstruction:
- May result from hypertrophied LV following relief of aortic stenosis.
- Treatment may include fluid resuscitation, systemic vasoconstrictors, and beta-blockade.
Aortic dissection.
Aortic annulus rupture (~0.5%):
- Clinical features may include hemorrhage, tamponade, and/or left ventricular myocardial failure.
- Consequences depend on the location of the rupture: (Sundt 2022)
  - Subannular rupture may cause a ventricular septal defect, mitral valve injury with subsequent mitral regurgitation, or a left ventricle to right atrium fistula.
  - Intra-annular rupture may cause coronary involvement.
  - Supra-annular rupture may cause intramural hematoma or frank ascending aortic rupture.
- Treatment depends on the site and severity of rupture. Deploying a second valve may sometimes be adequate, causing it to overlie the location of the rupture. Discontinue anticoagulation if possible, given the possibility of progression.

evaluation

ECG.
Echocardiography.
Chest radiography.
Laboratory evaluation:
- CBC.
- Coagulation studies.
- Basic chemistries (if not recently checked).
Occasionally, cardiac CT may be useful (e.g., to evaluate for aortic injury).

bleeding & vascular complications

hemorrhage

~15% may have major bleeding requiring surgical intervention.
Risk factors for bleeding include:
- Circumferential arterial calcification.
- Severely tortuous arteries.
- Percutaneous preclosure device failure. (Flynn 2020)
Bleeding typically results from access sites, e.g.:
- Femoral or iliac dissection.
- Retroperitoneal bleeding.
- Femoral pseudoaneurysm.
Management is similar to post-PCI bleeding, discussed here: 📖

other vascular complications

Arterial dissection (~5%), which may cause limb ischemia.
Pseudoaneurysm.

stroke

The risk of a clinically evident stroke has decreased to ~2%. (Bojar 2021)
Timing may be either acute or late.
- Acute predictors: procedural issues such as valve dislodgement.
- Late predictors: older age, chronic AF, history of stroke/TIA, atherosclerosis. (Flynn 2020)
The mechanism is embolic, often involving the MCA territory.

acute kidney injury

Acute kidney injury may result from hemodynamic fluctuations, atheroemboli, and/or intra-arterial contrast administration.

postoperative concerns after mitral valve surgery
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pulmonary HTN & RV dysfunction

Isolated RV failure can occur.
Selective pulmonary vasodilators may be helpful (e.g., inhaled pulmonary vasodilators or enteral sildenafil). (Bojar 2021)
Diuresis may be required for patients with pulmonary hypertension.

surgery for mitral regurgitation

Before repair, regurgitation causes afterload reduction of the left ventricle. Valve repair paradoxically exposes the LV to a higher afterload, which may lead to LV failure that requires inotropes and afterload reduction with vasodilators. A decrease in ejection fraction should be expected (but this is really just unmasking pre-existing LV dysfunction). (Bojar 2021)
Risk factors for postoperative LV dysfunction:
- EF <40%.
- LV dilation (LVESD >19 mm/m2).
- RV systolic pressure >45 mm.
- Ischemic etiology of mitral regurgitation. (Bojar 2021)

LV outflow tract obstruction (LVOTO)

Predictors of LVOTO include:
- Septal hypertrophy and/or small LV cavity. (Bojar 2021)
- Younger age.
- Male sex.
LVOTO may be induced by tachyarrhythmias, which impair diastolic filling.

hemodynamic parameters & rough targets
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perfusion targets

CI >~2.2 L/min/m2 is generally sufficient to maintain systemic oxygen delivery.
SvO2 >60%. (Bagchi 2025)
Skin perfusion (temperature, capillary refill time, absence of mottling).
Urine output >0.5 ml/kg/hr (however, urine output may be unreliable in intrinsic AKI).
Lactate <2 mM (may be directly elevated by epinephrine infusions).

MAP ~60-90 mm; SBP ~100-140 mm

Arguments for a higher Bp targets:
- Chronic HTN.
- Acute kidney injury.
- Acute ischemic stroke.
Arguments for a lower Bp targets:
- Low baseline BP.
- Concern for suture line integrity.
- Active bleeding.
- Systolic heart failure (afterload reduction).
- Mitral repair surgery. (Vives 2022)

CVP <~12 mm

CVP >~15 indicates RV failure. If encountered, further volume shouldn't be given, as this may exacerbate RV dysfunction (by increasing RV dilation). Instead, efforts should focus on improving RV function.

PAD (or PCWP)

The goal is for the filling pressures to be as low as possible while achieving other targets (ideally <20 mm).
15-20 mm might be a rough benchmark for patients with poor cardiac output. However, note that PAD/PCWP are static indicators that don't reveal fluid responsiveness (so a low PAD or PCWP doesn't necessarily indicate that fluid will improve cardiac output).
In diastolic dysfunction, higher filling pressures may be needed (e.g., PAD ~20-25 mm). (Bojar 2021)

heart rate

~80-110 b/m is often ideal to maximize perfusion. (Bagchi 2025)

cardiovascular deterioration, including low CO syndrome
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differential diagnosis of cardiovascular deterioration

reduced preload

Hemorrhage.
Hypovolemia (3rd spacing; cold diuresis).
Diastolic dysfunction (filling pressures are relatively inadequate).

obstructive cardiovascular physiology

Tamponade.
Tension pneumothorax.
Excessive PEEP/airway pressures.

excessive vasodilation

Vasoplegic syndrome.
Septic shock.
Adrenal shock (preoperative steroid discontinued).
Anaphylaxis (PRBC transfusion, medications).

LV failure

Myocardial stunning after cardioplegic arrest (aka low cardiac output syndrome).
- Myocardial function often deteriorates for ~6-8 hours after surgery, then gradually improves over about a day. (Bojar 2021) For patients with a lower initial EF and/or more complex operative course, myocardial recovery may occur more slowly. (Bagchi 2025)
Perioperative MI (including graft failure).

RV failure

Decompensated pulmonary hypertension.
RV myocardial infarction.
Suboptimal intra-operative RV protection (more common with retrograde cardioplegia). (Bagchi 2025)
Pulmonary embolism (uncommon in early post-op phase).

valvular dysfunction

Prosthetic valve dysfunction (e.g., paravalvular leak).
LV outflow tract obstruction (often following mitral surgery).
Papillary muscle rupture.
Aortic regurgitation (e.g., related to aortic dissection).

arrhythmia

Bradycardia.
Tachycardia.
Atrial arrhythmias with loss of atrial kick.

evaluation

bedside investigations

Physical examination (including temperature).
Chest tube drainage & pattern of drainage.
ECG:
- Ischemia?
- Arrhythmia?
Chest radiograph:
- Cardiogenic pulmonary edema?
- Pneumonia?
- Tension pneumothorax?
- Hemothorax?
Echocardiography (TTE +/- TEE).
Right heart catheterization data (if present).
Review medications (e.g., beta-blockers, diltiazem).

laboratory studies

Fingerstick glucose.
ABG/VBG.
Complete blood count.
Coagulation studies.
Electrolytes including iCa/Mg/Phos.

advanced testing

TEE.
CT angiography to evaluate for PE.

management: general hemodynamic optimization

treat any underlying etiologies, e.g.:

Rewarm.
Control arrhythmias.
Manage hemorrhage (PRBC transfusion, coagulation/source control).
Correct blood gas values.

volume management

General rules of thumb:
- [1] Avoid administering large volumes of crystalloid (e.g., >2 liters). (Bojar 2021)
- [2] Generally, diuresis should be avoided during the first six hours postoperatively unless there is cardiogenic pulmonary edema causing hypoxemia (ongoing third-spacing often occurs during this time frame). (Bojar 2021) Postoperatively, patients are often total body volume overloaded yet intravascularly depleted. Patients frequently require some fluid resuscitation during the first ~6 hours of their ICU course.
💡 Early extubation may help reduce fluid requirements by improving venous return. (Bojar 2021)

management of SVR & MAP

Target BP is discussed above: ⚡️
If SVR is excessive:
- Systemic vascular resistance may increase following surgery, possibly related to hypothermia.
- Vasodilators are most beneficial in the context of unequivocal systemic hypertension.
- Be careful when using vasodilators in patients with marginal cardiac output because an elevated SVR may be required to maintain adequate blood pressure. This situation may be suggested if the SVR is elevated but the MAP is within a normal range.
- Options for afterload reduction are discussed here: 📖
- With rewarming, patients may subsequently develop reduced SVR with vasoplegia (discussed below).
If SVR is inadequately low:
- Vasopressin is probably the most evidence-based selection here. The VANCS trial demonstrated that vasopressin reduced the incidence of severe complications or mortality after one month when managing vasoplegic syndrome (using a dose of up to 0.06 U/min). (27841822) Vasopressin is also especially useful in tachycardia or RV failure.
- Norepinephrine is often a reasonable choice that is easily titrated (especially if the cardiac output is borderline).
- Phenylephrine may be helpful in tachycardia or LVOTO (particularly if the patient's cardiac output is adequate).

management of systolic LV failure

Indications for inotrope:
- Patients most likely to benefit: CI <2 L/min/m2 despite optimized preload, afterload, and rhythm.
- SVI (stroke volume index) <30 ml/b/m2 implies poor myocardial function. (Bojar 2021)
Choice of inotrope:
- Epinephrine is usually a front-line choice (patients are often vasodilated postoperatively).
- Dobutamine (if there is high SVR).
- Milrinone (often 2nd line agent, added on to either dobutamine/epinephrine).

management of insufficient heart rate

External atrial pacing at ~90 b/m is often needed to optimize hemodynamics. (Bojar 2021)
Indications for pacing may include:
- Bradycardia (including 2nd/3rd degree block).
- Junctional heart rate.
- Normal heart rate (e.g., ~60-70 b/m) with inadequate perfusion despite other measures.
Pacing modality:
- [1] AAI pacing is generally ideal if the PR interval isn't excessively prolonged (to preserve synchrony and coordinated LV contraction).
- [2] AV pacing (e.g., DDD) may be the next-best option to preserve AV synchrony. If the native PR interval is >220 ms, DDD pacing with an A-V delay of 140 ms might improve cardiac output. (9327313) However, if the native QRS is narrow, transitioning from native conduction to RV pacing may compromise systolic coordination.

diagnose & treat RV dysfunction

Indicators of RV failure may include:
- Invasive hemodynamics:
  - CVP >15-18 mm (CVP/PCWP >0.6-0.8 suggests RV-predominant shock 📖).
  - PAPi <1-2. 📖
- Echocardiographic features:
  - IVC dilation.
  - RV dilation with reduced TAPSE. 📖
- POCUS indices of systemic congestion.
  - VExUS.
  - Femoral vein Doppler pulsatility indices. 📖
Treatments: 📖
- Normalize pCO2, pO2, and pH as able.
- Consider diuresis to optimize CVP.
- Inotrope therapy (e.g., milrinone > dobutamine).
- Support the MAP with agents that don't increase pulmonary vascular resistance (e.g., vasopressin).
- Inhaled pulmonary vasodilators.
- Enteral sildenafil.

mechanical cardiac support

If less invasive strategies fail, mechanical support may be needed.
Options may include IABP, Impella, and/or ECMO.

vasoplegic syndrome
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epidemiology

The rate overall may be ~5% after cardiopulmonary bypass.
Risk factors:
- Preoperative factors:
  - Advanced age.
  - LVEF <35% (RR up to 9). (36362635)
  - Preoperative renal failure.
  - Diabetes.
  - Anemia.
  - ACE inhibitor use.
  - Sepsis, surgery for infectious endocarditis.
- Operative factors:
  - Length of cardiopulmonary bypass & aortic cross-clamping.
  - Valvular surgery, transplantation, or LVAD.
  - Redo surgery.

definition

Basic defining characteristics:
- [1] Hypotension is resistant to fluid administration and usual doses of vasopressors (e.g., norepinephrine ~0.2-0.5 ug/kg/min).
- [2] Vasodilatory shock:
  - Systemic vasodilation:
    - SVR <800 dynes/cm5 (nl ~800-1200 dynes/cm5).
    - SVRi <1800 dynes/cm5/m2 (nl ~1900-2400 dyne-s/cm5).
  - Cardiac output is normal/high (CI >2.5 L/min/m2). (Bagchi 2025)
  - If a right heart catheter isn't inserted, echocardiographic evidence of a hyperkinetic left ventricle without other causes of shock is sufficient to diagnose vasodilatory shock.
Other aspects of vasoplegic syndrome:
- The vasoplegic syndrome can continue for >24 hours after surgery. (34161970)
Categorization of severity:
- Mild: MAP 50-60 mm and use of one vasopressor.
- Moderate: MAP 50-60 mm and use of two vasopressors.
- Severe: MAP <50 mm and use of two vasopressors. (34161970)

differential diagnosis

Septic shock.
Adrenal shock.
Anaphylaxis.
Pancreatitis.
Mesenteric ischemia.
Excess vasodilatory drugs.
Other forms of shock (vasodilatory shock may be a final common pathway for all types of shock). (Flynn 2020)

management

Fluid resuscitation:
- Fluid resuscitation may be considered if the patient is deemed to be hypovolemic, but in vasoplegic syndrome, fluid alone will not work. Fluid administration should generally be limited to 20-30 cc/kg maximum. (34161970)
- Transfusion to hemoglobin >9 mg/dL may be helpful by increasing blood viscosity. (36362635)
Vasopressin may be less arrhythmogenic and improve pulmonary vascular resistance.
- Vasopressin might be the most effective vasopressor for vasoplegia.
- The VANCS trial demonstrated that vasopressin reduced the incidence of severe complications or mortality after one month. The dose of vasopressin used was up to 0.06 U/min.
- For post-cardiac surgery vasoplegia, the vasopressin dose may be increased to 0.1 U/min (6 U/hour). (Bojar 2021) However, it might be desirable to avoid doses above 0.06 U/min. (36362635)
Norepinephrine provides some inotropy and chronotropy. Norepinephrine is often started initially as a front-line vasopressor. However, an absent/minimal response to catecholamine vasopressors is a hallmark of vasoplegic syndrome – so by definition, norepinephrine alone will fail. (Bagchi 2025)
Stress-dose steroid (hydrocortisone 50 mg IV q6hr).
Methylene blue: 💉 One RCT suggested a mortality benefit for norepinephrine-refractory vasoplegia. (14759425)
Hydroxocobalamin. 💉 Some data suggest that a gradual infusion of five grams over six hours may allow for more sustained efficacy. (33242823)
Angiotensin 2.
- Starting dose: 20 ng/kg/min. (Bagchi 2025)
- Risks include an increased rate of thromboembolic events.

tamponade & pericardial effusion
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epidemiology of tamponade

General epidemiology:
- Incidence may be ~1-8% of patients.
- Tamponade usually presents in the first 12 hours. (Bagchi 2025) However, it can present acutely or insidiously for up to ~10 days postoperatively. (Flynn 2020)
- Tamponade may follow the removal of epicardial pacing wires. (15193929)
Causes:
- Surgical bleeding (e.g., leaking grafts).
- Coagulation abnormalities (e.g., capillary ooze).
Risk factors include:
- Coagulopathy (e.g., elevated PTT preoperatively).
- Postoperative anticoagulation and/or antiplatelet agents.
- Early postoperative bleeding requiring blood products.
- Renal failure.
- Urgent surgery, more complex operations (e.g., valve surgery, surgery for endocarditis). (Bojar 2021)

clinical manifestations & diagnosis of tamponade

Onset may be abrupt or insidious.

suspicious clinical features are sometimes seen

Chest drains:
- Blood draining from mediastinal drains suddenly stops (due to drain obstruction).
- Blood output suddenly increases.
Dyspnea may occur (if the patient can report this).

hemodynamics: low-output shock

General findings can include:
- Hypotension.
- Narrow pulse pressure.
- Reduced urine output (insidious tamponade may sometimes present with low urine output, since the kidneys are affected by both the low cardiac output and systemic venous congestion).
- Tachycardia (but this may be muted by beta-blockade).
Pulsus paradoxus (inspiratory fall in SBP >10 mm). 📖 This may be better appreciated on an arterial line tracing.
CVP:
- CVP elevation can occur if the clot compresses the RA and/or RV.
- CVP waveform may show tall A- and V-waves (with absent or diminished Y-descent). (33564995, Vives 2022)
Wedge pressure might be elevated if left-sided chambers are compressed (except during early inspiration and expiration).
Femoral vein Doppler might theoretically help by revealing right ventricular dysfunction.
(Diastolic equalization often won't occur because a localized pericardial clot often occurs, affecting only some chambers.)

ECG changes

ECG lacks sensitivity.
Decreased voltage compared to prior ECG may be seen.
(Further discussion of ECG in pericardial effusion here: 📖)

chest radiograph

Chest radiography lacks sensitivity (it's usually unremarkable).
In ~20% of cases, mediastinal widening may be seen. ⚡️

echocardiography

IVC dilation without collapse usually occurs (right-sided tamponade).
Pericardial effusion (note the quantity and quality).
Diastolic collapse of cardiac chambers.

CT scan

CT scanning may be appropriate for stable patients, especially if it allows evaluation of other competing diagnoses.
High-attenuation blood products can be readily identified.
Tamponade physiology is less effectively evaluated by CT scan as compared to echocardiography. However, tamponade physiology may also be suggested by dilation of the vena cava and underfilling of the ventricles. (31731897)

differential diagnosis: causes of tamponade & pericardial effusion

Hemopericardium.
Small postoperative pericardial effusion:
- This may occur in up to ~80% of patients.
- Effusion is usually seen by the second postoperative day but may develop later.
- Effusions are generally small and clinically insignificant.
Postpericardiotomy syndrome ➡️.

management

Temporary stabilization may sometimes be achieved with:
- Volume administration.
- Vasopressors.
Urgent surgical exploration is generally preferred.
Percutaneous drainage:
- It may sometimes be an option for late effusions. (Sundt 2022)
- Percutaneous drainage won't be effective for the removal of clots.

hypertension
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causes of postoperative hypertension may include

Hypothermia.
Shivering.
Pain/anxiety/agitation with the lifting of general anesthesia.
Underlying chronic hypertension.
Hypercapnia or respiratory distress.
Hypoglycemia.
Vasopressors.
Volume overload.
Status post SAVR with improvement in cardiac function.
- HTN often occurs several hours after ICU admission.

assessment may include

Core temperature?
Signs of anxiety/pain/dyspnea?
Hemodynamic evaluation (including volume status).
Review chest radiograph & ABG/VBG data (? hypercapnia or active respiratory failure).
Review glucose trends.
Review home antihypertensive regimen.

treatment goals

Target BP is discussed in the section above on hemodynamic optimization. ⚡️

management

⚠️ Be cautious with the use of long-acting medications in the immediate postoperative period, as patients often transition into a hypotensive/vasoplegic state.
[1] Treat any identifiable causes of HTN (e.g., pain/anxiety, ventilator dyssynchrony).
- Strongly consider the possibility of untreated pain/agitation/delirium.
- If hemodynamic data indicates volume overload, consider diuresis.
- Using propofol as an antihypertensive for short periods may be acceptable (if there isn't access to clevidipine and immediate intubation isn't anticipated).
[2] Vasodilator:
- Short-acting vasodilators are often helpful in the early postoperative period since hypertension is frequently due to excessive systemic vascular resistance. However, vasodilator utilization may be limited by tachycardia or diastolic hypotension (e.g., status post AVR).
- Nicardipine 📖 or clevidipine 📖: workhorse agents for afterload reduction.
- Nitroglycerine 📖: reasonable choice if volume overload is present.
- Nitroprusside 📖: titratable venous & arterial vasodilator, but requires very close monitoring (arterial line) and limited doses to avoid toxicity.
[3] Beta-blocker:
- Beta-blockers are generally recommended after cardiac surgery to prevent AF.
- Beta-blockers may be helpful for:
  - Hyperdynamic heart with plenty of cardiac output (often seen in patients with normal LV function and/or LVH).
  - Coincident tachycardia (e.g., AF with RVR).
  - Patients status post AVR. (Bojar 2021)
- Options include:
  - IV metoprolol 📖
  - IV labetalol 📖
  - Esmolol infusion 📖.

postoperative atrial fibrillation & flutter: prevention
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epidemiology

General risk factors:
- Age might be the strongest risk factor (~25% risk at 60YO; ~40% risk at 70YO; ~50% risk at 80YO). Age alone may predict POAF as accurately as many scoring scores to predict POAF risk. (38505057)
- History of AF.
- Heart failure (systolic or diastolic; dilated left atrium).
- Preoperative P-wave duration >116 ms.
- Redo surgery.
- COPD.
- Diabetes, obesity, OSA.
- Renal failure.
- Hypokalemia, hypomagnesemia.
- Alcohol use disorder.
- Inotropic medication use.
- Beta-blocker withdrawal.
Risk related to surgery type:
- Isolated CABG: ~30% incidence.
- Isolated valvular surgery: ~40%.
- CABG plus valvular surgery: ~50%. (Flynn 2020)
- Proximal aortic surgery: 30-50%. (38505057)

natural history

AF develops most frequently within the first few days following surgery (especially between postoperative days #2-4). (Dabbagh 2018)
New-onset AF is usually self-limited, with spontaneous cardioversion to sinus rhythm often occurring within one day. >90% of patients will be in sinus rhythm after 1-2 months.

POAF prevention: general measures

Dexmedetomidine may reduce the risk of AF.
Avoidance of high-dose inotropes (as able).

[1/3] magnesium

Meta-analyses have generally found that IV magnesium reduces the risk of POAF. (38505057)
A validated dose is 2 grams of IV magnesium sulfate daily for 3 days postoperatively. (15620927) This may be infused slowly to maximize cellular uptake (rather than renal excretion).
Magnesium levels may also be monitored. However, note that serum levels often don't track well with intracellular magnesium levels. For atrial fibrillation treatment, a target serum magnesium level is often 3.6-4.9 mg/dL. Thus, even if the serum magnesium level is >2 mg/dL, IV magnesium may remain beneficial.
In the absence of renal failure or myasthenia gravis, it would be unlikely that 2 grams of IV magnesium daily would cause side-effects.
Besides AF, aggressive magnesium repletion may also reduce the risk of torsade de pointes. There is also evidence that IV magnesium could have some analgesic and anti-shivering effects.

[2/3] amiodarone

Indications:
- [1] Amiodarone may be combined with beta-blocker. It's unclear whether amiodarone should be used for all patients or only for higher-risk patients. (Bojar 2021) Amiodarone has been independently associated with a reduction in stroke rate, causing the ESC/EACTS guidelines to recommend amiodarone or beta-blockers for POAF prevention. (38505057)
- [2] Amiodarone might also be useful for patients unable to tolerate beta-blockade.
Timing:
- Therapy should ideally be started well before surgery to establish an adequate drug level (e.g., 400 mg PO BID beginning the week before surgery). (9400034)
- Postoperatively, 400 mg PO BID for 4-6 days, followed by 200 mg daily, might be a reasonable dose. Enteral administration of amiodarone may cause less bradycardia, hypotension, or QT prolongation than IV administration. (38505057)
- Intravenous amiodarone may be utilized for patients unable to take oral medication.
  - 0.5 mg/hour infusion equates to 720 mg/day amiodarone, roughly equivalent to an oral dose of 400 mg BID.

[3/3] oral beta-blocker

Beta-blockers are often recommended as a front-line preventative agent (Class IA).
This is especially important for patients who were on beta-blockers before surgery (to avoid beta-blocker withdrawal).
Indications: Should be utilized unless contraindicated (e.g., bradycardia, hypotension, pressor dependence, or low cardiac output state).
Timing:
- Most studies on beta-blockers involved starting therapy following surgery. (Flynn 2020) Initiating therapy as soon as possible after surgery may increase efficacy.
- Often, beta-blockers are initiated the first postoperative morning. (Bojar 2021)
Agent:
- Metoprolol 12.5-50 mg BID may be reasonable (depending on patient specifics).
- Carvedilol may be more effective but also causes more significant hypotension.
- For patients previously on beta-blockers, consider their prior dosing regimen.

postoperative atrial fibrillation & flutter: management
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initial AF stabilization package

Wean down beta-adrenergic vasopressors as able.
For hypotension, consider vasoconstrictors that don't cause beta-stimulation (e.g., vasopressin, phenylephrine).
Optimize volume status.
Treat pain, anxiety, or withdrawal states (dexmedetomidine may decrease heart rate).
Treat hypokalemia and/or hypomagnesemia.
Treat hypoxemia or excessive work of breathing.

management: rate vs. rhythm control

Studies have generally found similar outcomes from either rate or rhythm control so that this decision may be personalized based on the patient.
Indications to consider rhythm control (chemical or electrical cardioversion):
- Rate control is difficult to achieve.
- AF causes symptoms.
- AF causes hemodynamic instability (especially in pulmonary hypertension or diastolic dysfunction).
- AF persists >24-48 hours (in efforts to reduce the risk of stroke and avoid anticoagulation). (Flynn 2020)
- AF plus WPW.
- Atrial flutter (flutter is more amenable to cardioversion or overdrive pacing and less amenable to rate control).
- The patient is intubated (making electrical cardioversion easier and safer).

management: rhythm control

DC cardioversion:
- Successful in ~95% of patients.
Chemical cardioversion:
- IV magnesium may promote cardioversion. (8504578)
- Amiodarone is often a reasonable option.
- Ibutilide is another option for some patients. 📖
If an internal atrial wire is present, atrial flutter may be cardioverted by overdrive pacing.

management: rate control

Beta-blockers are often preferred (to combat elevated sympathetic tone in the postoperative state).
- Esmolol ⚡️ may be utilized if there is concern about tolerating beta-blockade.
- IV metoprolol ⚡️ is another option.
- Many patients may already be on a low-dose beta-blocker.
IV amiodarone is a second-line agent for reducing the ventricular rate. Amiodarone might be preferred among patients who are more hemodynamically tenuous.
Diltiazem ⚡️ could be considered in the context of hypertension or vasospasm. Compared to metoprolol, diltiazem has vasodilatory properties (which may increase a propensity for hypotension) and lacks efficacy in promoting conversion to sinus rhythm.

management: anticoagulation

Anticoagulation should be considered for recurrent paroxysmal AF or for AF persisting longer than 24-48 hours.
The risks of bleeding must be weighed against the risk of stroke.
- The CHA2DS2-VASC score may help risk-stratify the risk of stroke. 🧮 However, the risk of stroke after cardiac surgery is lower than for general non-valvular AF. (38505057) Overall, AF may increase the stroke risk from ~1.2% to 2.7%, an absolute risk increase of ~1.5%. In POAF, the stroke risk appears to increase when the CHA2DS2-VASc score is ≧4. (38505057)
- The risk of bleeding in the immediate post-operative context is generally substantial.

postoperative monomorphic VT (or polymorphic VT due to ischemia)
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epidemiology

General risk factors:
- Prior MI.
- Heart failure.
- Reduced LVEF.

specific etiologies of ventricular arrhythmia status post-cardiac surgery

Acute MI.
Electrolyte abnormalities:
- Hypokalemia or hyperkalemia.
- Hypomagnesemia.
Medications:
- Inotropes.
- Withdrawal of antidysrhythmic medication.
Right heart catheter that has migrated into the right ventricle.
Sepsis.
Anemia.

magnesium prevention of ventricular arrhythmia

Meta-analysis demonstrated that magnesium supplementation decreases the risk of ventricular arrhythmia by 50%.

treatment of sustained monomorphic VT

Unstable: cardioversion.
Stable:
- Lidocaine is often a first-choice agent. It might also have the advantage of providing postoperative analgesia.
- Amiodarone may be preferable among patients with ventricular dysfunction. (Dabbagh 2018) Amiodarone can also simultaneously prevent or treat atrial arrhythmias (especially atrial fibrillation).
The underlying cause(s) should be addressed.
- Causes of VT/VF or ventricular ectopy: 📖

bradyarrhythmias
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Bradyarrhythmias are especially common after valvular surgery.
Temporary pacing via wires placed at surgery may be utilized for stabilization.
Anticholinergics (atropine or glycopyrrolate) are usually ineffective in the postoperative setting. (Dabbagh 2018)
Permanent pacemaker insertion is required in ~2% of patients. If bradycardia is persisting for days, consider the need for a permanent pacemaker.

atrial electrography (AEG)
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The easiest way is to attach V1 to one of the atrial wires (yielding a unipolar atrial lead) when obtaining a 12-lead ECG. (34712508) Attaching the atrial lead to a unipolar (precordial) lead preserves the remainder of the ECG.
How to interpret an AEG:
- [1] Start by identifying ventricular QRS complexes (based on comparison to V2). Ventricular QRS complexes may be unusually small on the AEG.
- [2] Any superimposed deflections reflect the atrial activity. Sometimes, these deflections may be very large.
Some tips:
- AF may appear more organized and regular on AEG than expected (example: 📸).
- Ventricular tachycardia may occur with 1:1 retrograde conduction, or there may be more ventricular depolarizations than atrial depolarizations (example: 📸). If there are more ventricular depolarizations than atrial depolarizations, this proves it is VT (not SVT with aberrancy).

epicardial pacing
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pacemaker calibration

evaluation for capture

General:
- Turn the pacemaker 10 beats above the intrinsic rate.
- Increase mA until every pacing spike achieves capture. This is the capture threshold.
- Set the output (mA) to twice the determined threshold plus one.
Epicardial pacemaker leads:
- The capture threshold should generally be <5 mA. (37600212)
- If the capture threshold is >10 mA, consider placing a transvenous pacemaker. (Bojar 2021)

evaluating sensitivity & setting the sensitivity threshold

Only assess this in a patient with an intrinsic rate >40-50 b/m.
- If there is no endogenous rhythm, the sensitivity is typically set to 2 mV. (17300304)
Set the pacer output to 0.1 mA and reduce the pacemaker rate to 10 b/m below the intrinsic rate.
Decrease the sensitivity (raise the mV) until the sense indicator stops flashing and the pace indicator starts flashing.
Slowly increase the sensitivity (reduce the mV) until the sense indicator flashes continuously. This is the sensing threshold.
Set the sensitivity to half of the sensing threshold (mV/2).
⚠️ Concerningly low sensitivity threshold:
- Suggested by a ventricular threshold <2 mV or an atrial threshold <1 mV.
- If the pacemaker sensitivity is set to half of this threshold (1 mV in the ventricle or 0.5 mg in the atrium), this will be very low – which may lead to over-sensing.

troubleshooting

failure to pace (no pacemaker spike)

Diagnosis:
- A pacemaker is not discharging at all when it should be.
- No pacemaker spikes are visible on the monitor.
- The pacemaker box isn't blinking “pace.”
Causes:
- Oversensing, e.g., detection of:
  - Electrical activity from the other cardiac chambers.
  - Senses the T-wave.
  - Shivering or rigors.
  - Electrocautery.
- Disconnection:
  - Wire migration.
  - Lead fracture.
  - Disconnection from pacing box.
Troubleshooting:
- Check all connections (consider replacing the connecting cable).
- Try reducing sensitivity (increasing the sensing threshold).
- Try asynchronous pacing:
  - This will work if the problem is oversensing, but will fail if the issue is disconnection.
  - It may be helpful emergently if the patient is pacemaker-dependent.

failure to capture (spike but no capture)

Diagnosis:
- The pacemaker is discharging but not capturing the myocardium.
- The pacemaker box is blinking “pace.”
- Pacemaker spikes may be discernable on the monitor.
Causes:
- Disconnection:
  - Fibrosis around the pacemaker leads.
  - Electrode displacement.
  - Wire fracture.
  - Disconnection from the pacemaker box.
- Myocardial refractoriness:
  - Ischemia/infarct.
  - Electrolyte abnormalities (especially hyperkalemia).
  - Medications (e.g., antiarrhythmics, beta-blockers, lidocaine). (17381573)
- Pericardial effusion. (37600212)
- Atrial fibrillation (atrial pacing only).
Troubleshooting:
- Try increasing the current.
- Check all connections (consider replacing the connecting cable).
- Evaluate for pericardial effusion or electrolyte abnormalities.
- Reversing polarity may sometimes improve the capture threshold.
- Convert to a unipolar pacemaker:
  - Red(+) lead coming from the pacer box: Ground this on the patient's body (connect to a surface ECG electrode or an 18G needle placed in the skin).
  - Black(-) lead coming from the pacer box: Connect to the (+) temporary epicardial wire or to both of the temporary epicardial wires. (Bojar 2021)
- Use a chronotrope to increase the intrinsic rate and/or improve the myocardial sensitivity to pacing stimuli.
- If all else fails, default to alternative therapy (e.g., transcutaneous and/or transvenous pacing).

failure to sense (causes excess beats, R-on-T)

ECG findings: Pacemaker spikes occur right before, during, or after P/QRS complexes.
Causes:
- [1] The sensing threshold is set too high.
- [2] Similar etiologies as failure to capture (see above).
- [3] Inappropriate pacemaker settings (e.g., excessive refractory periods). (17381573)
Troubleshooting:
- Evaluate the sensing threshold (consider reducing the sensing threshold).

atrial pacing (AAI or AOO)

modes for atrial pacing

AAI may be used.
AAO may be used:
- AOO must be set significantly above the intrinsic rate.
- There is a risk of pacing atop an endogenous P-wave, causing AF. This risk is lower in patients with bradycardia.
- AOO may be advantageous if there are issues with over-sensing, such as electrocautery (especially in the context of asystole or atrial bradycardia, where pacing on top of an endogenous P-wave is unlikely).

indications for atrial pacing

Endogenous sinus heart rate is lower than desired.
Suppression of PACs and/or PVCs (the set rate comes before ectopic beats have time to occur).
Prevention of AF.

risks/drawbacks of atrial pacing

[1] Atrial pacing depends on an intact conduction system. If a third-degree heart block occurs, AAI or AOO will not protect the patient from asystole.
[2] If atrial tachyarrhythmias occur, AAI/AOO modes won't achieve much.
[3] Atrial pacemakers may not sense a PVC, so there may be a risk that they could deliver a beat right afterward, causing an R-on-T phenomenon. However, this is unlikely because in this scenario, the AV node will usually be refractory, so it will block the atrial beat. (17381573)

atrioventricular pacing (AV; usually DDD)

indications for AV pacing

3rd degree (complete) heart block.
2nd degree heart block (achieves 1:1 conduction).
1st-degree heart block: If the native PR interval is >220 ms, then DDD pacing with an A-V delay of 140 ms might improve cardiac output. (9327313)
Any indication for atrial pacing (listed above) if there is a desire for a backup ventricular pacemaker (e.g., in the event of a 3rd-degree heart block).

AV interval

[a] Patient is receiving dual chamber pacing (e.g., due to a high-grade AV block):
- AV interval of 150 ms may be reasonable.
- An individual patient might benefit from a longer or shorter AV interval (e.g., 100 ms to ~225 ms). (17381573) This interval may be manually adjusted to optimize hemodynamics.
[b] Increasing AV interval to encourage native conduction:
- For patients with a narrow QRS complex (<120 ms), native AV conduction may improve LVEF.
- A longer AV interval may be selected to encourage native AV conduction (e.g., AV interval of ~200 ms). If the AV interval is longer than the patient's endogenous A-V conduction, DDD mode functions identically to AAI mode (the ventricular wire merely functions as a backup ventricular pacemaker).
Ventricular Safety Pacing:
- This feature is intended to avoid ventricular oversensing (which could be caused by cross-talk from atrial activity). Ventricular oversensing could cause failure to pace – leading to asystole.
- If a ventricular signal is detected very early after atrial activity, the pacemaker may be confused about whether it is atrial or ventricular (e.g., a PVC). The pacemaker will fire rapidly, earlier than it was set to fire (with a reduced AV interval). This is safe whether the sensed signal is an atrial or ventricular signal (the pacemaker fires rapidly enough to avoid an R-on-T phenomenon). (36180288)

DDD mode

DDD allows synchronization with the atria.
If an atrial arrhythmia occurs, the pacemaker may work poorly (e.g., transmitting tachycardia).
- Setting an upper rate limit may temporarily protect against this.
- For persistent atrial arrhythmias, DDI mode may be superior to DDD (discussed below).
Pacemaker-mediated tachycardia:
- This may result if retrograde AV conduction creates a macro-reentry loop along with the pacemaker.
- Potential management:
  - [i] DVI mode may be utilized if the pacemaker is significantly faster than underlying atrial activity.
  - [ii] PVARP setting: postventricular atrial refractory period setting. This helps prevent the retrograde P-wave from being misinterpreted as intrinsic atrial activity.
    - A very long PVARP will limit the maximal atrial tracking rate, but this isn't a problem for ICU patients (it is more of an issue for exercising outpatients). (17381573)

DVI mode (AV sequential, ventricular inhibited)

DVI senses only the ventricle (if a ventricular beat occurs, no pacing is delivered).
- DVI could be conceptualized as a combination of AAO + VVI.
DVI pacing may be helpful if there is no atrial activity or a slow atrial rate. The DVI pacer rate is set faster than the intrinsic sinus rate, so that the pacemaker will produce synchronized AV conduction.
DVI mode is simpler than DDD mode, which avoids problems related to atrial sensing in DDD mode:
- Atrial over-sensing may cause dropped atrial beats and loss of AV conduction.
- Atrial under-sensing may cause an atrial beat to fall on top of a native QRS complex. This is extremely dangerous because the pacemaker is blanked to detection of the QRS complex while the A-lead is firing. So, the pacemaker will not realize that a native QRS beat occurred. This may cause the pacemaker to trigger the ventricle after the native QRS complex, leading to an R-on-T phenomenon.
  - 💡Safe pacing with DDD or DDI mode requires accurate atrial sensing.
- Avoidance of pacemaker syndrome.
Limitations to DVI mode:
- Similar to AAO, there is a risk of triggering AF if the atrial rate is high enough to compete with the pacing rate.
- Contraindicated in atrial tachyarrhythmias. (17381573)

DDI mode (AV sequential, non-P-synchronous, with dual chamber sensing)

DDI mode is a dual mode designed to handle tachyarrhythmias:
- The pacemaker does nothing if atrial and ventricular rates are above the threshold.
- If the atria and/or ventricular rates are too slow, the pacemaker will pace.
- The pacemaker will not be stimulated by atrial activity (unlike DDD pacing, which will entrain the atrial activity at higher rates). Native atrial contraction will inhibit atrial pacing, but it won't stimulate ventricular pacing.
- The set AV interval will only occur if atrial and ventricular activity rates are slower than the set rates (in this situation – if the heart is passive – then DDI mode will resemble DDD mode). (37600212)
Advantage: DDI may be superior to DDD for the management of rapid atrial arrhythmias. Permanent pacemakers in DDD mode will generally automatically switch to DDI mode if they detect an excessively fast atrial rate. (17381573)
Limitation: DDI is unable to accommodate a physiologically appropriate sinus tachycardia. (17381573)

ventricular pacing (VVI)

indications/advantages of VVI mode

[1] AF/Flutter with slow ventricular rate.
[2] Management of pacemaker syndrome.
[3] Backup mode for patients in whom bradycardia might occur (VVI is a simple mode, so it is less likely to malfunction in a patient who doesn't need anything fancy).
[4] Overdrive suppression of PVCs. (17381573)

anti-tachycardia pacing

⚠️ basic properties of anti-tachycardia pacing

[1] Consider pre-treatment with antiarrhythmic medications, for example:
- Atrial flutter: magnesium and/or antiarrhythmic (e.g., amiodarone, ibutilide).
[2] Be sure that the atrial wires are attached (not the ventricular wires) and that these wires aren't inadvertently capturing the ventricles:
- Pacing initially 10-15 beats above the ventricular rate will clarify whether the ventricle is inadvertently being captured.
- Use the same energy you will use for overdrive pacing (e.g., 20 mA).
- ⚠️ If the atrial wires capture the ventricle, overdrive pacing could induce VT/VF.
[3] The patient should be on a monitor, able to defibrillate if needed.

atrial flutter

Overdrive pacing is effective in typical (type I) flutter (<320-340 b/m), but not atypical (type II) flutter with faster rates. (17381573)
Settings:
- Set the current to maximal amplitude (e.g., 20 mA).
- Set the rate to ~30 b/m higher than the atrial flutter rate. (37600212)
Application of atrial overdrive pacing:
- Apply for up to 20-60 seconds.
- A change in P-wave morphology may indicate capturing the atria (e.g., atrial complexes become positive).
- The goal is to terminate the arrhythmia with the lowest amount of overdrive pacing, so it may be reasonable to begin with some shorter bursts of overdrive pacing.
Abruptly stop overdrive pacing:
- Ideally, a sinus rhythm will ensue (sometimes following a pause).
- Atrial fibrillation can occur (which may be short-lived).
- Sinus bradycardia can occur (requiring pacing).

junctional tachycardia

Junctional tachycardia is common after cardiac surgery, often with rates ~100-120 b/m.
Junctional tachycardia can be overdrive suppressed by pacing at 120% of the junctional rate in various modes (e.g., AAI or DDD). Once the tachycardia is overdrive suppressed, the pacemaker rate may be gradually reduced. When the pacemaker rate falls below the endogenous sinus rate, sinus rhythm may be re-established. (17381573)

AVNRT

AVNRT can be terminated using “underdrive” pacing (below the SVT rate) or “overdrive” pacing (above the SVT rate).
After capture, the rate may be gradually reduced to the desired target. (17381573)

epicardial lead removal

Removal may occur off anticoagulation entirely or on a low level of anticoagulation (depending on the clinical scenario). This should happen before the initiation of a NOAC.
There is a small risk of tamponade and/or mediastinal bleeding (~1/1000).

differential diagnosis includes:

MI.
Pericarditis.
Pneumothorax.
Pneumonia.
Pulmonary embolism.
Sternal woundinfection.
Aortic dissection.
GERD.
Musculoskeletal/incision pain.

evaluation may include:

Examination:
- Friction rub?
- Evidence of wound infection?
ECG.
Chest radiograph.
Occasionally: Echocardiography, CT angiography.

perioperative & postoperative MI
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presentation

postoperative MI is fairly common

After CABG: ~5%. (37345559)
After isolated mitral valve surgery: ~2%. (37345559)

presentations may include

⚠️ Symptoms are often impossible to evaluate (due to intubation and sedation). Even if the patient is extubated, some postoperative chest pain is expected, so anginal chest discomfort may be difficult to discern.
Chest pain is out of proportion to expected pain.
Arrhythmia:
- Ventricular arrhythmias.
- Bradycardia (inferior MI).
Hemodynamic instability:
- Hypotension.
- Low cardiac output syndrome.
- Unusually high pressor requirements.
Cardiogenic pulmonary edema.

diagnosis

ECG

It may be confounded by postoperative pericarditis.
New pathological Q-waves support an MI. However, these are seen in ~5% of patients after surgery and may not be associated with significant cardiac biomarker elevation. Instead, some Q-waves may result from altered depolarization or unmasking of prior infarcts. (Bojar 2021)

troponin

Troponin is generally elevated after cardiac surgery.
Various sources and guidelines recommend elevating the troponin cutoff value (e.g., 5-10 times the usual cutoff). However, this will vary depending on local troponin assays.

echocardiography

It may help detect the development of new focal wall motion abnormalities.

ECG-gated coronary CT

Good sensitivity for graft occlusion (sensitivity and specificity >95%). (25173653)
It is not generally utilized, but it may be an option in certain cases.

etiologies of MI

graft-related after CABG (60% of post-CABG MI)

Twisting/kinking.
Tension.
Dissection.
Anastamotic stenosis.
Acute thrombosis.
Vasospasm (~5%).
Competitive flow.

non-graft related

Incomplete revascularization (~5%).
Nonspecific cardioplegia-related (ischemia-reperfusion)(~30%; catheterization unremarkable).
Distal microembolization of debris or air (e.g., air embolism may occlude the RCA).
New native coronary artery lesion (~4%). (37345559)
Coronary artery injury.
- Aortic valve surgery or TAVR: the valve may obstruct low-lying coronaries.
- Mitral valve surgery: posterior stitches come close to the circumflex artery. Additionally, oversizing of the valve can compress the circumflex artery.
- Tricuspid valve surgery: risks injury to the RCA (right coronary artery).
- Aortic root surgery: re-implantation of coronary ostia may lead to coronary embolization or anatomic distortion. (Flynn 2020)
- Coronary dissection from instrumentation (including osteal cardioplegia cannulae). (Sundt 2022, 37345559)

management of MI

supportive therapies

Reduction in blood pressure may decrease myocardial workload:
- Beta-blocker if the patient is sufficiently stable.
- Nitrates may be used (and potentially serve a dual function of treating vasospasm).
Transfusion to a higher hemoglobin target may be considered. ⚡️
Suspected coronary vasospasm:
- Nitroglycerine infusion may be considered if there is suspicion of coronary vasospasm (starting at 0.5 ug/kg/min and increasing as tolerated). Infusions of diltiazem and nicardipine may be added as well if hemodynamically able.
- Milrionine is the inotrope of choice here since it causes coronary vasodilation.
- Correct hypomagnesemia.
- If ECG changes persist, emergency catheterization is indicated to identify and possibly correct the problem.
- After stabilization, oral coronary vasodilators may be utilized (e.g., isosorbide mononitrate 20 mg daily, nifedipine 30 mg q6hr, diltiazem CD 180 mg daily, or amlodipine 5 mg daily). (Bojar 2021)

interventional therapies

Indications for coronary angiography are not well defined but could include: (37345559)
- ECG findings (e.g., STE, new left bundle-branch block, other patterns suggesting occlusive MI).
- Echocardiography showing new regional wall motion abnormality.
- Electrical instability (VF, cardiac arrest, multiple episodes of sustained ventricular tachycardia).
- Low cardiac output syndrome despite usual postoperative support (e.g., CI <2 L/min/m2, mixed venous saturation <60%).
- Substantial elevation in cardiac biomarkers.
Percutaneous coronary intervention is challenging for several reasons (stenting of vein grafts can be difficult; dual antiplatelet therapy increases bleeding risk in post-CABG patients). However, PCI is often the best approach as it can be performed rapidly.
Repeat CABG is another option; this will depend on patient-specific anatomy.

aortic dissection
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Dissection is rare with conventional on-pump CABG:
- Aortic cannulation: ~0.05% incidence.
- Axillary or femoral cannulation site: ~0.5% incidence. (Bagchi 2025)
Risk factors may include:
- Age >60 years old.
- Chronic hypertension.
- Severe atherosclerosis of the ascending aorta.
- Underlying aortic dilation.
Potential presentations may include:
- Recognition during surgery (ideally).
- Tamponade.
- Aortic regurgitation.
- Hemorrhage.
- Regional ischemia of branch vessels.

glycemic control
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Targeting a glucose level of 110-180 mg/dL seems reasonable.
Glucose should initially be monitored hourly and eventually spaced out to q2-3 hours. (Flynn 2020)
Continuous insulin infusion is often preferred, given more reliable bioavailability.
STS guidelines recommend an insulin infusion initiated in the OR for diabetic patients and continued for at least 24 hours postoperatively to target a glucose <180 mg/dL.
A continuous insulin infusion protocol is located here: 📖
(Rationale: Hyperglycemia correlates with poor outcomes. However, there is little high-quality evidence to establish that tighter glycemic control causes improved outcomes.)

use of steroids after cardiac surgery

Summary of evidence:
- Prophylactic steroid use might reduce perioperative bleeding as well as post-operative nausea/vomiting. (12760978)
- A recent RCT of perioperative high-dose dexamethasone (1 mg/kg) found reduced ICU length of stay without effects on other outcomes. (38904693)
- A historic study demonstrated that massive steroid doses were pretty well tolerated (a gram of methylprednisolone!). (15999046)
- A systematic review and meta-analysis of RCTs found that: (29576107)
  - Mortality wasn't statistically different, but there was a beneficial trend with steroid administration (3% vs. 3.5%).
  - Myocardial injury was more likely in the steroid group (8% vs. 7%).
  - New onset AF was lower in the steroid group (25.7% vs. 28.3%).
Whether some dose of steroid should be utilized routinely remains unclear.
If a patient has another indication for steroid (e.g., adrenal insufficiency, organ transplantation), cardiothoracic surgery isn't a contraindication to steroid use.

acute adrenal insufficiency

Rarely, cardiac surgery may cause acute adrenal insufficiency due to adrenal hemorrhage (e.g., associated with aggressive heparinization during cardiopulmonary bypass).
Manifests of acute adrenal insufficiency may include:
- Flank and/or abdominal pain.
- Nausea/vomiting, diarrhea.
- Fever.
- Vasodilatory shock (which may be refractory to fluid and vasopressors).
Investigations and treatments are described in the chapter on adrenal crisis here: 📖

hypothyroidism
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Surgery reduces levels of thyroid hormones. T3 and free T3 remain low for up to six days, whereas T4 often returns to normal within a day. (Bojar 2021)
Uncontrolled preoperative hypothyroidism may promote reduced cardiac output, bradycardia, and occasionally difficulty weaning off mechanical ventilation (decompensated hypothyroidism).
Management:
- Patients with chronic hypothyroidism should be maintained on their dose of thyroid replacement.
- For patients with decompensated hypothyroidism, more aggressive treatment may be beneficial. 📖

approach to abdominal pain
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causes include

Gastritis.
Cholecystitis (calculus or acalculous).
Perforation (usually gastric/duodenal ulceration).
Pancreatitis.
Mesenteric ischemia.
C. difficile.
Ileus or severe constipation.
Obstruction.
Urinary:
- Bladder distension.
- Pyelonephritis.
Retroperitoneal hematoma. (Bojar 2021)

evaluation may include

Review of prior medical history (especially prior GI pathology).
Serial abdominal examination.
Laboratory testing:
- Liver function tests.
- Lactate level.
- Lipase.
- C. difficile (for diarrhea).
Radiology:
- Abdominal X-ray.
- RUQUS.
- CT angiography (evaluate entire abdomen and mesenteric perfusion).

epidemiology

Extremely common in the immediate postoperative period.
Ileus usually resolves within a few days postoperatively.

clinical manifestations

Distension.
Pain (however, severe pain suggests the possibility of a more malignant process such as mesenteric ischemia or pancreatitis).
Nausea/vomiting.
Tube feeding intolerance.

diagnosis of ileus

Abdominal radiograph.
POCUS.

management of ileus

Limit opioids by using a multimodal pain strategy.
Consider opioid antagonists (e.g., oral naloxone).
Early mobilization
Treat electrolyte abnormalities
Hold feeding temporarily
NG suction only if needed for the management of symptoms
Prokinetics are generally ineffective, but neostigmine may be considered if there is simultaneous colonic involvement.
Suppositories and enemas may be utilized.

colonic pseudo-obstruction (Ogilvie syndrome)
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epidemiology

Occurs in up to 3.5% of patients. (Dabbagh 2018)

clinical manifestations

Distension.
Pain.

diagnosis

[1] The abdominal radiograph reveals colonic distension.
[2] Differential diagnosis includes mechanical obstruction or C. difficile colitis with toxic megacolon. CT scan should be considered to exclude alternative diagnoses.

treatment

Neostigmine is generally front-line therapy. The primary complication of concern with neostigmine administration is bradycardia. If neostigmine is truly infused at the proper rate (2 mg over five minutes), this complication is infrequent. However, for patients with epicardial pacing leads, it would be rational to connect them with a pacemaker box with a backup rate in case bradycardia did occur.
Some emerging data supports the utilization of physostigmine.
(Further discussion: 📖)

GI bleeding
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epidemiology & causes

Upper GI bleed (~90-100%): (38616788)
- Usually due to stress ulceration (duodenum > gastric). (Dabbagh 2018)
- Coagulopathy may contribute.
Lower GI bleed (<10%):
- Hemorrhoids (statistically most common). (38616788)
- Mesenteric ischemia.
- Ischemic colitis.
- C. difficile colitis.
- Exacerbation of bleeding from a polyp/tumor/AVM/diverticula due to coagulopathy.

clinical manifestation

Hypotension, hypovolemic shock.
Falling hemoglobin.
Upper GI bleed is suggested by:
- Melena, hematochezia, hematemesis.
- Gastric tube return may be bloody (if the patient has a gastric tube in place).
Lower GI bleed is suggested by:
- Bright red blood per rectum (especially with clots).
- Gastric tube return should not be bloody.

management

Reversal of coagulopathy as able.
PRBC transfusion.
Proton pump inhibitor.
Upper endoscopy may be considered.
For lower GI bleeding, CT angiography may be obtained with a view to potential interventional radiology intervention.
(Further discussion of management of GI bleeding: 📖)

mesenteric ischemia
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pathophysiology

[1] NOMI (nonocclusive mesenteric ischemia) is the most common cause, reflecting hypoperfusion.
[2] Less common etiologies include:
- Embolism to the superior mesenteric artery.
- Acute thrombosis of an atherosclerotic plaque.
- Mesenteric venous thrombosis (possibly from HIT). (Bojar 2021)

epidemiology

Incidence is ~0.5% (38616788)
It may occur within hours to several days after surgery. (Dabbagh 2018)
Risk factors include:
- Older age.
- Extensive atherosclerosis, peripheral vascular disease.
- Atrial fibrillation.
- Aortic cross-clamp time >100 minutes.
- IABP use.
- Low cardiac output.
- Use of two or more vasoconstrictors.

clinical manifestations are often nonspecific

Septic shock.
Abdominal pain (which may be out of proportion to abdominal examination findings).
Abdominal distension, ileus.
Feeding intolerance, nausea/vomiting.
Diarrhea, sometimes with GI bleeding.
Persistently elevated lactate (but in general, this is a poor diagnostic study for mesenteric ischemia).

diagnosis

Physical examination is usually unimpressive (unless peritonitis has already developed).
CT angiography of the abdomen.

management

Resuscitation.
Reduce the dose of vasoconstrictors as much as possible.
Antibiotic therapy.
Consider IV heparin if it is safe to do so.
Consultation with vascular surgery +/- interventional radiology:
- Embolectomy if possible.
- Nonocclusive mesenteric ischemia can be treated by interventional radiology placement of a catheter into the superior mesenteric artery with regional infusion of vasodilators.
- Laparotomy and bowel resection if required by perforation, necrotic bowel, or abdominal compartment syndrome.

pancreatitis
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epidemiology

Clinically overt pancreatitis is rare (rate <0.5% of patients). (Bojar 2021)
Usually, pancreatitis occurs slightly later than other gastrointestinal complications (with an average onset of nine days after surgery). (Dabbagh 2018, 38616788) The pathogenesis may involve hypoperfusion, often occurring in the context of multi-organ failure.

clinical manifestations

Vasodilatory shock state that can mimic septic shock.
Abdominal pain.
Nausea and vomiting.
Abdominal distension, paralytic illeus.

diagnosis of pancreatitis ideally requires two of the following

Lipase elevation above three times the upper limit of normal (note that elevated amylase is nonspecific, so amylase levels are not helpful in diagnosing pancreatitis).
CT abdomen.
Symptoms consistent with pancreatitis.

management of pancreatitis

Treatment is primarily supportive.
Resuscitation is similar to sepsis resuscitation (for patients with hemodynamic instability).
Analgesia.
Discontinue any potentially causative medications.
(Further discussion on the treatment for pancreatitis: 📖).

acalculous cholecystitis
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epidemiology

Acute cholecystitis occurs after ~0.2-0.5% of cardiac surgeries. Of these, the majority are due to acalculous cholecystitis. (38616788)
Often, it is a delayed complication in the context of critical illness.
Often occurs ~10-15 days postoperatively. (Dabbagh 2018)

clinical manifestations

Right upper quadrant pain.
Septic shock.

diagnosis

Right upper quadrant ultrasonography.
CT scan.
HIDA scan is generally unhelpful for acalculous cholecystitis.
(Further discussion: 📖)

management

Antibiotics.
Percutaneous drainage is generally preferable.
(Further discussion: 📖)

evaluation of the bleeding patient

radiologic studies to look for blood

Chest radiograph:
- Pleural effusion?
- Mediastinal widening?
POCUS:
- Evidence of pericardial tamponade?
- Intraperitoneal free fluid?
- Hemothorax?

coagulopathy evaluation: lab tests to consider

Complete blood count.
TEG.
Ionized calcium level (iCa).
PTT (elevation may reflect heparin rebound or consumption of coagulation factors).
INR.
Fibrinogen level.
Anti-Xa level (May help quantify the significance of heparin rebound).

TEG interpretation for patients with clinical bleeding

🏆 Viscoelastic testing (TEG or ROTEM) has been shown to reduce PRBC transfusion and the need for redo surgery caused by coagulopathy. (31445833)
R-time (heparinase TEG):
- Normal value: 5-10 minutes.
- R-time >12 minutes suggests coagulation factor deficiency (with potential benefit from FFP or PCC).
The difference in R-time between native TEG and heparinase TEG:
- This deviation reflects heparin activity (which may occur in heparin rebound).
- If the native R-time is >125% of the heparinase R-time, consider protamine.
MA (maximal amplitude):
- Normal value: 50-70.
- MA <40-48 may be actionable in a patient with bleeding. (33708416) MA seems important: low post-operative MA may predict bleeding better than other coagulation parameters (including platelet count, fibrinogen, or INR). (16884984)
- Low MA may reflect thrombocytopenia, hypofibrinogenemia, or both. Functional fibrinogen assessment may help determine which product(s) to use if this assay is available. When in doubt, starting with fibrinogen administration is often reasonable (since fibrinogen carries fewer side effects and is longer-lasting than platelet transfusions).
% Fibrinolysis (LY-30):
- The normal value is 0-3%. (31263903)
- LY-30 >3% could suggest benefit from a fibrinolytic inhibitor in the context of active bleeding.

(TEG platelet mapping)

Platelet mapping may be considered if there is a recent ASA or P2Y12 administration, but this is limited by turnaround time.
Among patients treated with clopidogrel before surgery, TEG with platelet mapping was shown to predict bleeding more accurately than the number of days since discontinuation of clopidogrel. (21126640)
TEG with platelet mapping appears accurate and helpful in determining platelet function and guiding transfusion status post-cardiac surgery.

interventions to consider for ongoing bleeding

[1] hypothermia control

[2] control basic chemistries

pH management.
iCa target >1 mM.

[3] PEEP & BP

[a] PEEP elevation may encourage cessation of bleeding from capillaries and veins. (Bagchi 2021)
[b] Target SBP ~90-100 mm may be reasonable in the face of active bleeding.
- (HTN management is discussed above: ⚡️).

[4] platelet-fibrinogen-DDAVP axis

Platelets and fibrinogen interact synergistically to promote clot formation, so to a certain extent, one deficiency may be compensated for with an excess of the other. With the TEG-5000 system, the MA (maximal amplitude) reflects the combined function of platelets and fibrinogen.
Fibrinogen:
- Usual fibrinogen targets might be:
  - General target post-CTS: >100 mg/dL.
  - Active bleeding: target >150 mg/dL.
  - Refractory hemorrhage: could target >200 mg/dL.
- Reduced MA on TEG may suggest potential benefit from fibrinogen, especially if platelet count is adequate (discussed above).
- Fibrinogen may be repleted using:
  - Cryoprecipitate. 📖
  - Fibrinogen concentrate. 📖
Platelet targets:
- Usually target >50,000 in the immediate postoperative period. However, some sources say >20,000-30,000 is OK in the absence of bleeding. (Bojar 2021)
- Indications to target >100,000 might include:
  - Ongoing bleeding despite a platelet count >50,000.
  - Patients who received antiplatelet agents (e.g., aspirin, P2Y12 inhibitors, GPIIb/IIIa inhibitors).
  - Uremia.
- TEG: A reduced MA may suggest a potential benefit from platelets, especially if the fibrinogen level is adequate. Alternatively, a normal MA on TEG (>50) argues against the potential benefit of platelet transfusion.
DDAVP: Potential indications overlap with the indications for platelet transfusion:
- Thrombocytopenia (especially if platelet transfusion is challenging).
- Uremia.
- Antiplatelet agents (e.g., clopidogrel within 5 days, ticagrelor within 3-5 days, or prasugrel within 7 days). (33251719)
- Cardiopulmonary bypass run >140 minutes.
- TEG with low MA (maximal amplitude).
- Demonstrated platelet dysfunction. (Bagchi 2025)

[5] protamine 💉

Protamine may be used to treat heparin rebound.
Indications may include:
- Elevated anti-Xa levels.
- TEG shows heparin effect (as discussed above).

[6] fibrinolytic inhibitor (tranexamic or aminocaproic acid)

This could be indicated for elevated LY-30 on TEG (as discussed above).

[7] coagulation factors (FFP or PCC)

These are indicated for:
- Prolonged R-time on the TEG following heparinase administration (“heparinase TEG”).
- Substantially prolonged INR (if TEG isn't available).
Dosing strategies:
- FFP 📖
- PCC 📖

[8] PRBC transfusion

This depends on HgB and bleeding activity.
Transfusion targets are discussed in the section below.

[9] rough potential indications for surgical exploration

Continuous bleeding via chest tube:
- >500 ml in the first hour postoperatively (but this may depend on how well the pleura was drained during the procedure).
- >400 ml/hr for 2 hours.
- >300 ml/hr for 3 hours.
- >200 ml/hr x 4 hours (Alternatively: ~100-200 ml/hr for several hours is often OK if this settles down over time). (Bojar 2021)
- >1000 ml total bleeding in first four hours postoperatively. (Sundt 2022)
- ⚠️ Turning or moving patients may sometimes cause chest tubes to dump out blood that accumulated over time. Clues that this is occurring may include dark blood and the absence of ongoing blood drainage. (Bojar 2021)
Sudden massive bleeding.
Evidence of a large pericardial or pleural effusion in the setting of hemodynamic changes.
Any evidence of tamponade (discussed above: ⚡️)

pathophysiology: coagulopathies which may occur after cardiopulmonary bypass

Hypothermia.
Hypocalcemia.
Acidosis.
Hemodilution.
Loss/consumption of coagulation factors.
Fibrinogen abnormality:
- Low fibrinogen level.
- Ongoing hyperfibrinolysis (may be caused by cardiopulmonary bypass).
Platelet abnormalities:
- Thrombocytopenia, often due to:
  - Heparin utilization (non-immune HIT).
  - Cardiopulmonary bypass (dilution and consumption of platelets).
- Acquired platelet dysfunction: Cardiopulmonary bypass causes alpha-granule depletion and reduction in platelet surface glycoproteins (GPIb and GPIIb/IIIa). (32955756)
- Uremia may worsen platelet function.
Medications, most often:
- Heparin: Heparin rebound occurs in up to 50% of patients due to redistribution of heparin away from protamine (especially in patients with obesity or with very high doses of heparin). This may be managed by re-dosing protamine (usually with 20-25% of the initial dose). (Dabbagh 2018)
- Protamine: Protamine itself may inhibit platelet function and stimulate clot breakdown. (Flynn 2020)
- Antiplatelet medications.
- NOACs (residual effects may linger with older age, renal/hepatic dysfunction).
Aortic valve replacement patients may have von Willebrand syndrome (Heyde syndrome: platelet activation due to high-velocity jet of aortic stenosis causes acquired von Willebrand's disease).

PRBC transfusion targets
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transfusion targets: summary

The ERAS guidelines recommend a restrictive transfusion strategy with a hemoglobin target of >7.5 mg/dL. (38284956) However, there is some equipoise regarding this, so tailoring transfusions to individual patients' needs may be rational.
Additional factors to consider when determining the benefit of transfusion may include the following:
- [1] Evidence of active myocardial ischemia.
- [2] Volume status:
  - If the patient is being diuresed, the hemoglobin may tend to drift up.
  - If the patient is volume-depleted, transfusion could improve volume status.
- [3] Presence of any active blood loss.
- [4] Perfusion indices:
  - DO2/VO2 ratio (which can be calculated 📖).
  - Mixed venous oxygen saturation.
- [5] Vasoplegic syndrome (higher hemoglobin level may increase blood viscosity and improve blood pressure). (36362635)

evidence on transfusion targets

TITRe2 Trial (2015) (25760354)
- Multi-center RCT involving 2007 patients undergoing cardiac surgery.
- Randomized to transfusion target of 7.5 vs. 9 mg/dL.
- There was no difference in the primary endpoint (a complex composite endpoint).
- Mortality was higher in the restrictive group (4.2% vs. 2.6%, p = 0.045).
TRICS-III trial (2017) (29130845)
- Multi-center RCT involving 5243 patients undergoing cardiac surgery.
- Randomization to transfusion target of 7.5 vs. 9.5 mg/dL in the critical care arena (with a lower transfusion target of 8.5 mg/dL for patients in the non-ICU ward).
- There was no difference in the primary endpoint (a complex composite endpoint).
- Mortality was lower in the restrictive group (3% vs. 3.6%, not statistically significant).

IV iron for the management of iron deficiency

The literature supports the use of IV iron to manage iron deficiency preoperatively. Ideally, this would be administered preoperatively, allowing hematopoiesis before surgery.
Iron deficiency may be discovered postoperatively in patients who undergo urgent/emergent surgery. IV iron may still offer some benefits for these patients. (39332997) Diagnosis and treatment of iron deficiency is discussed here: 📖.

anticoagulation regimens
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⚠️ Anticoagulation regimens will vary depending on patient and procedure specifics. The following section merely provides a general description of commonly utilized anticoagulation regimens.

CABG

Aspirin:
- Recommendations indicate aspirin should be administered to post-CABG patients to improve outcomes. Aspirin is often started 6-24 hours after surgery. (Bojar 2021)
- Platelets may be less responsive to aspirin after cardiopulmonary bypass, so higher doses might be reasonable (e.g., 325 mg QD).
- Aspirin should be held among patients with thrombocytopenia.
- For patients with aspirin sensitivity, clopidogrel may be utilized instead (300 mg loading dose followed by 75 mg daily). (Bojar 2021)
DAPT may be considered for:
- Off-pump CABG (Level I recommendation).
- Drug-eluting stent placed within <1 year.
- CABG for acute coronary syndrome.
- CABG for stable ischemic heart disease (to reduce vein graft occlusion; weakest indication).

surgically implanted tissue valve(s)

Aspirin:
- Most patients: aspirin 75-100 mg indefinitely.
- AVR and MVR: start aspirin 325 mg daily after three months.
Warfarin:
- Most patients: target INR 2.5 for 3-6 months if there is a low risk of bleeding.
- AVR and MVR: target INR 3 for 3-6 months.

TAVR

Usual therapy:
- DAPT for 6 months with aspirin 81 mg QD and clopidogrel (although this may not be required for patients at high bleeding risk).
- After six months, stop clopidogrel and continue on aspirin monotherapy.
For patients with low bleeding risk, warfarin may be utilized.
For patients with AF, anticoagulation (warfarin or NOAC) is recommended alone, without an antiplatelet agent. (Bojar 2021)

mechanical valve(s)

Aspirin:
- The guidelines disagree. For most patients, aspirin 81 mg daily may be used only if there is atherosclerotic disease or a history of embolism. However, some guidelines do recommend aspirin 81 mg daily for all patients.
- AVR-MVR: aspirin 75-100 mg daily.
Warfarin:
- AVR: target INR 2.5 indefinitely.
- MVR: target INR 3 indefinitely.
- AVR-MVR: target INR 3.4.5 indefinitely.
- INR targets may vary somewhat depending on the specific type of valve.

warfarin initiation guideline

Day 1:
- 2.5 mg if: underweight/malnourished, >75 years old, hepatic dysfunction, interacting medications (amiodarone, antibiotics).
- 5 mg if none of the above.
Day 2:
- INR <1.5 = 2.5-5 mg.
- INR 1.5-1.9 = 1.25-2.5 mg.
- INR >1.9 = 0 mg.
Day 3:
- INR <1.5 = 5-7.5 mg.
- INR 1.5-1.9 = 2.5-5 mg.
- INR 2-3 = 0-2.5 mg
- INR >3 = 0 mg.
Day 4:
- INR <1.5 = 7.5-10 mg
- INR 1.5-1.9 = 5-7.5 mg.
- INR 2-3 = 0-5 mg.
- INR >3 = 0 mg.
Day 5:
- INR <1.5 = 10 mg.
- INR 1.5-1.9 = 5-10 mg.
- INR 2-3 = 0-5 mg.
- INR >3 = 0 mg.
Day 6:
- INR <1.5 = 10-12.5 mg.
- INR 1.5-1.9 = 7.5-10 mg.
- INR 2-3 = 2.5-5 mg.
- INR >3 = 0 mg. (Bojar 2021, UpToDate)

management of supratherapeutic warfarin:

Without bleeding: 📖
With active bleeding: 📖

fever following cardiac surgery
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causes of fever after cardiac surgery

Infections:
- [#1] Pneumonia (including VAP)(~4%). ⚡️
- [#2] Wound infection (~2-3%).
  - Deep sternal wound infection.
  - Post-venotomy cellulitis.
  - Chest tube sites.
  - Pacing wire sites.
- [#3] Line infection (~1%).
- [#4] Urinary tract (~0.5%).
- [#5] Endocarditis, especially involving prosthetic valve (~0.2%).(Vives 2022)
- C. difficile.
- Acalculous cholecystitis.
- Empyema.
- Pre-existing infection (e.g., endocarditis with metastatic spread).
Non-infectious fever:
- Benign postoperative fever (post-operative day #1-3; usually <39C/102F). Especially in the first 24-48 hours postoperatively, fever is nonspecific.
- Aspiration pneumonitis.
- Drug fever.
  - Dexmedetomidine (causes fever in ~5% of patients, increasing risk with ongoing infusion). 📄 (29137584)
- Pulmonary embolism (usually low-grade fever, <39/102). (10631196)
- PCIS (post-cardiac injury syndrome). ⚡️
(Expanded differential diagnosis of fever in ICU is here: 📖)

evaluation of fever after cardiac surgery

History:
- Are there any localizing symptoms? Diarrhea?
Physical examination:
- Respiratory (if intubated: Sputum? Increasing ventilator support?).
- Abdominal tenderness?
- Skin exam:
  - Evaluate surgical incision.
  - Evaluate any line/drain sites.
Chest radiograph. (IDSA 2023)
Blood cultures.
- Two sets of peripheral blood cultures at different sites.
- Any line in place >48-72 hours should also be cultured. (18379262)
- 🚨 For patients with fresh valves or vein grafts, there should be a reduced threshold for initiation of antibiotics in response to a single positive blood culture.
Urinalysis with culture if:
- Foley catheter in place with prolonged/unexplained fevers (if the Foley functions adequately, this would be a rare etiology of fever). (23878765, 18379262)
- The Foley catheter has been removed, and the patient has urinary symptoms.
C. difficile testing for diarrhea.
CT scan(s) may be indicated by:
- Clinical abnormalities (e.g., abdominal pain).
- Suspected pulmonary embolism.
- Abnormal chest radiograph that requires clarification.
- Recent instrumentation/surgery, persistent fever, and no alternative explanation for the fever.
Inflammatory markers:
- These are often more useful for discontinuing antibiotics (not for diagnosing infection). (A general discussion of inflammatory markers is here: 📖)
- CRP may be elevated by surgery, but persistent elevation >100 mg/L beyond four days suggests infection. (Vives 2022)
- Procalcitonin typically peaks on POD1 and then returns to <1 ng/mL by ~POD3. (Vives 2022) Note that some noninfectious complications may elevate procalcitonin, such as mesenteric ischemia. (38616788)
(Expanded evaluation of fever in the ICU is here: 📖)

sternal wound infection
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definition

This includes both infection of the sternum and/or mediastinum.

epidemiology

~1% rate following CABG surgery.
Usually diagnosed within the first two weeks postoperatively (median of one week).
Risk factors may include:
- Patient-related:
  - Diabetes.
  - Obesity (BMI >40).
  - Prior myocardial infarction.
  - Smoking, COPD.
  - Aortic calcification.
  - Older age.
  - Malnutrition.
- Procedure-related:
  - Combined CABG/valve surgery.
  - Aortic surgery.
  - Cardiopulmonary bypass time.
  - Re-exploration for bleeding.
  - Respiratory failure.
  - Use of bilateral internal mammary artery.
- Postoperative complications:
  - Mediastinal bleeding, re-operation.
  - Multiple blood transfusions.
  - Prolonged intubation.
  - Low cardiac output states.
  - Acute kidney injury.
  - Refractory hyperglycemia.
  - Central line-related bacteremia (relative risk of 5). (Bojar 2021)

clinical features

The acuity of the infection:
- Staph aureus tends to present within the first 10 days after surgery.
- Coagulase-negative Staph. usually presents later and more insidiously. (Bojar 2021)
Depth of the infection:
- Minor/superficial infections: may cause tenderness, erythema, purulent drainage, and localized wound breakdown. The sternum itself is usually stable.
- Major/deep incisional infections (including deep subcutaneous, osteomyelitis, and mediastinitis) may include the above features, but also usually with an unstable sternum.
Other symptoms may include:
- Fever (often the first finding).
- Tachycardia.
- Chest pain.

radiology

Chest radiograph may show sternal dehiscence:
- [1] Mid-sternal stripe sign (>3 mm is suspicious).
- [2] Sternal wire displacement (present in most patients with dehiscence; often precede clinical detection). (15193929)
CT scan is superior.
- Findings may include mediastinal fluid collections, abscess, gas, and sternal dehiscence.
- However, detecting some fluid and gas may be expected in the postoperative period. This is more suspicious if it occurs >2 weeks postoperatively or if changes worsen. (25173653, 30300004)
- In some cases, CT may detect features of spreading infection (e.g., pericardial effusion, empyema, abscess). (30300004)
- PET-CT scan may help clarify the presence of true infection. (Vives 2022)

laboratory studies

Gram-positive bacteremia: Sternal wound infection accounts for >50% of gram-positive bacteremia. (Bojar 2021)
Purulent drainage should be cultured.
Wound aspiration may be utilized to confirm infection and direct antibiotics if there is no spontaneous drainage.

management

Antimicrobial therapy:
- Most frequent organisms:
  - Gram-positive: Staphylococci (including coag-negative Staph), Streptococci.
  - Gram-negatives, including Pseudomonas and Enterobacter spp.
- Prolonged therapy may be required.
- Ideally, therapy should be guided by culture results (as discussed above).
Wound management:
- Minor/superficial infections: oral antibiotics, opening the wound, and local wound care may suffice. (Bojar 2021)
- Major/deep sternal wound infection: Surgical management often involves debridement, drainage, open packing, and delayed closure. (Dabbagh 2018)

prognosis

Associated with high mortality (~10%).

leg wound infection
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clinical presentation

Various presentations may include:
- Cellulitis (often begins along the medial aspect of the mid-tibial region at the venectomy site).
- Wound breakdown with purulent drainage.
- Indurated wound overlying an endoscopic tract, often with an associated hematoma. (Bojar 2021)
Infection may cause high fevers and systemic toxicity (which typically reflect streptococcal cellulitis).

differential diagnosis

DVT.
Infection of implanted devices (e.g., prosthetic vascular graft).

management

Wound management may involve:
- Removal of suture material.
- Hematoma drainage and/or debridement of necrotic skin.
Antimicrobial management: Involved pathogens are generally gram-positives, especially beta-hemolytic streptococci.

C. difficile
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signs and symptoms include

Diarrhea.
Abdominal pain.
Abdominal distension.
Fever.

diagnosis

Based on stool analysis.
There should be a low threshold to test for C. difficile (to allow for early treatment and infectious precautions).
Treatment algorithms vary between hospitals – use whatever tests are typically utilized at your center.

treatment

Initiation of empiric oral vancomycin is reasonable if there is a high index of suspicion.
Monitor carefully for the development of toxic megacolon (a surgical emergency).
(Further discussion of treatment is here: 📖).

dexmedetomidine

Advantages:
- RCTs demonstrate that it causes a reduced risk of renal failure (OR 0.66). (37453497)
- It may reduce delirium.
- Associated with more rapid ventilator weaning (dexmedetomidine may be continued throughout the weaning and extubation process, which can be helpful in some patients with agitation upon awakening).
- Provides some analgesia.
- It may reduce the rate of post-operative AF (OR 0.76). (36535747)
Disadvantages:
- Sympatholytic effects increase the risk of bradycardia and reduced cardiac output.
- Tachyphylaxis and dependency/withdrawal may occur after several days.

propofol

Advantages:
- May achieve a deeper level of sedation.
- It is easier to titrate more rapidly.

discussion of various agents

scheduled acetaminophen 💉

This is safe and mildly beneficial.
For optimal analgesic benefit, a high dose should be scheduled:
- Most patients: 1,000 mg q6hr.
- Severe alcoholism, stable cirrhosis, or weight <50 kg: 2 grams/day (650 mg q8hr). (25477978)
- Avoid entirely in acute liver injury or decompensated cirrhosis.
Administration of 1,000 mg acetaminophen q6hr has been demonstrated to reduce opioid consumption and pain following cardiothoracic surgery in RCTs. (27521969) The DEXACET RCT showed that scheduled acetaminophen reduced rates of delirium. (30778597)
IV acetaminophen may be utilized for patients lacking enteral access.

scheduled pregabalin

Dosing:
- 150 mg PO BID may be a standard dose, although lower doses may be considered in the elderly. (32892818)
- Dose reduction for renal failure:
  - GFR 30-60 ml/min: 75 mg BID.
  - GFR 15-30 ml/min: 75 mg daily.
Evidentiary basis:
- Pregabalin (150 mg BID) for two weeks in combination with ketamine (0.1 mg/kg/hr for 48 hours) was shown in an RCT to reduce pain (including chronic pain), reduce opioid consumption, and improve long-term quality of life. (31149930; full study results are here) 75 mg BID also has shown efficacy in RCTs, including a reduction in chronic pain. (21474474)
- Meta-analyses support the ability of pregabalin to reduce length of stay and decrease morphine consumption. (33763487)
Side effects may include dizziness, visual alteration including diplopia, and sedation. (32892818)
Pregabalin may be preferable to gabapentin in terms of more rapid and consistent absorption and more predictable pharmacokinetics. The evidentiary support for pregabalin is much more robust than for gabapentin (which was found to delay extubation in some studies).

low-dose ketamine infusion 📖

This may be helpful in various situations, including:
- [1] In combination with pregabalin to reduce chronic pain.
- [2] Among patients with ongoing pain despite acetaminophen and low-dose PRN opioids.
- [3] Ketamine has antidepressant effects that could improve postoperative neuropsychiatric outcomes and promote patient participation in early mobilization and rehabilitation. Ketamine is not generally utilized in the ICU solely as an antidepressant, although this has been described.
Commonly used doses for pain include 0.1-0.2 mg/kg/hour.
Neuropsychiatric effects may occur in a dose-dependent fashion (generally at doses >0.12 mg/kg/hr). These are often pleasant but can sometimes cause anxiety. Co-administration with sedatives (e.g., dexmedetomidine or propofol) decreases the propensity for causing anxiety.
(Further discussion of ketamine: 📖)

PRN opioids

Initially, PRN opioids may be administered by nursing (e.g., 0.5 mg IV boluses of hydromorphone).
PCA (patient-controlled analgesia) may be helpful once patients are sufficiently conscious, often morphine (further discussion on PCA use and dosing: 📖).
Opioid infusions should be avoided since these tend to produce tolerance and withdrawal. 🌊
The risks of excessive opioid use include:
- Constipation, ileus, nausea.
- Delirium. To avoid delirium, care should be taken to ensure that opioids are being utilized to treat pain rather than being nonspecifically used for the management of agitation (ideally, using a behavioral pain scale).
- Respiratory depression.
- Analgesic tolerance, hyperalgesia, chronic pain, and chronic opioid use. (32892818)

alpha-2 agonists

[#1] Dexmedetomidine is often used initially to provide sedation and analgesia. As discussed above, dexmedetomidine is well supported by evidence for post-cardiac surgery patients.
[#2] Following extubation, tizanidine or clonidine could be considered for patients who seemed to benefit substantially from dexmedetomidine (based on a similar mechanism of action). These are sympatholytic agents, so they are contraindicated in hypotension, shock, or bradycardia. However, if patients tolerate dexmedetomidine, then they are likely to tolerate low enteral doses of tizanidine or clonidine.
- Clonidine 💉 has some analgesic effects, along with greater sedative and hemodynamic effects.
- Tizanidine 💉 has predominantly analgesic and muscle relaxant effects, with relatively fewer hemodynamic effects.
- There is no substantial evidence supporting these agents in post-cardiac surgery patients, but their benefit may be inferred among individual patients based on mechanistic similarity with dexmedetomidine.

agents to avoid

NSAIDs are avoided due to the potential for adverse cardiac events, increased bleeding, renal failure, and stress ulceration. These are suboptimal for critically unwell patients.

background discussion

pain after cardiac surgery

The pain usually peaks over the first two days and declines gradually through POD6. (32892818)
There are numerous sources of pain (sternal wound, intercostal nerve pain, vein harvesting wounds in the legs, back/limb stiffness, chest drains, endotracheal tube, nasogastric tube).
One-third of patients have chronic pain, which persists >6 months after surgery. (32892818)
Consequences of inadequate analgesia may include:
- Depression.
- Reduced mobility and coughing (causing atelectasis, respiratory failure, and DVT).
- Insomnia, delirium.
- Increased risk of chronic pain. (39141254)

principles of multimodal analgesia after cardiac surgery

The use of low doses of multiple agents provides synergy and avoids the need for high doses of opioids. Opioid-sparing strategies have been shown to accelerate extubation and reduce ICU length of stay. (32892818)
Preemptive initiation of analgesics may improve analgesia and avoid pain crises that require high-dose opioids. (32892818) This especially applies to less potent agents (e.g., acetaminophen, pregabalin), which are unlikely to have substantial efficacy when used in a PRN fashion for paroxysms of pain.

postoperative nausea & vomiting
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risk factors

Female sex.
Nonsmoker.
History of postoperative nausea/vomiting or motion sickness.
Postoperative opioid use.

agents for treatment

Ondansetron is often a front-line agent.
Olanzapine is an excellent choice if available.
Prochlorperazine is another good 2nd line agent.
(More on antiemetics: 📖)

risk factors for delirium

Age.
Preoperative use of neuroactives (e.g., alcohol, opioids, benzodiazepines, antipsychotics).
Preoperative neurological disorders (e.g., CVA, Parkinson disease, dementia).
Preoperative medical comorbidities (e.g., peripheral vascular disease, chronic kidney disease, malnutrition).
Severe cardiac disease; complex and prolonged surgical procedures.
Pre-existing white matter hyperintensities on MRI (thought to represent chronic microvascular disease). (Bagchi 2025)

differential diagnosis includes

Hypoglycemia
Hypercapnia.
Electrolyte abnormalities (e.g., dysnatremia).
Medication effects:
- Sedatives.
- Analgesics.
- Antiemetics.
- Anesthetic agents.
Withdrawal syndromes (e.g., alcohol, gabapentin, benzodiazepines).
Uremia.
Sepsis.
Stroke (ischemic, hemorrhagic, watershed hypoperfusion).
Seizure.
Congestive encephalopathy.
Wernicke encephalopathy.

evaluation

Examination, including neurologic evaluation.
Laboratory studies:
- STAT fingerstick glucose.
- Electrolytes.
- ABG/VBG if hypercapnia is possible.
- Medication review (both home & hospital medications).
More advanced studies:
- CT angiography.
- EEG to evaluate for seizure (seizures are discussed further below).
(Additional information on delirium evaluation: 📖)

management may include such measures as:

Treatment of any specific etiologies that have been identified, including:
- IV thiamine if Wernicke encephalopathy is possible.
- Correction of any contributory electrolyte abnormalities (especially dysnatremias).
Medication reconciliation, often with the continuation of home neuro/psych meds.
Early mobility.
Multimodal analgesia and sedation (see sections above).
- Dexmedetomidine may be especially useful to manage hyperactive delirium and promote restorative sleep with a normal circadian rhythm.
Antipsychotics may also be used to treat agitation, nausea/vomiting, and/or promote sleep:
- Haloperidol 💉 (often front-line for severe agitation; increases QT; antiemetic).
- Olanzapine 💉 (no effect on QT; longer-acting; PO/IV administration; antiemetic).
- Quetiapine 💉 (oral and slow-onset, may be used to promote sleep, not helpful in acute agitation).

ischemic stroke
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risk factors

Patient-related:
- Atrial fibrillation.
- Prior stroke or TIA.
- Atherosclerosis (e.g., aorta, carotid, intracranial arteries, peripheral vascular disease).
- Vascular risk factors:
  - Older age.
  - Diabetes.
  - Hypertension.
  - Hyperlipidemia.
  - Smoking.
- Renal failure.
- Low cardiac output syndrome, moderate/severe left ventricular dysfunction.
Procedure-related:
- Mitral valve replacement.
- Dual valve replacement.
- Intraoperative hypotension.
- Emergency surgery. (Flynn 2020, Bagchi 2025)

mechanism & classification

Mechanisms may include:
- Embolic.
  - Cardioembolic.
  - Emboli arising from carotid/intracranial atherosclerosis.
- Hypoperfusion.
- Atrial fibrillation.
- Thrombosed prosthetic valve.
- Endocarditis.
- Left ventricle mural wall thrombus.
Classification:
- Early: apparent on emergence from anesthesia.
- Delayed: neurologic deficit developing >24 hours postoperatively. A stroke clearly occurring after surgery implies a mechanism with a greater likelihood of recurrence. This often reflects AF, or patients with known cerebrovascular disease plus low cardiac output states. (Bojar 2021)
- Late: develops >1 month postoperatively.

neuroimaging

CT scan is the study of choice (including CT angiography and perhaps even a CT perfusion study).
MRI may be impossible among patients with epicardial pacing leads and/or a right heart catheter.

management

Consider stroke code activation if feasible.
Thrombolysis is contraindicated (absolutely contraindicated for two weeks and relatively contraindicated for three months). (Flynn 2020)
Endovascular therapy should be pursued per usual protocols for large vessel occlusions.
Blood pressure management:
- Avoid hypotension or hypoperfusion.
- Permissive hypertension may be desirable from a stroke standpoint (if tolerated from a cardiac standpoint). BP targets in ischemic stroke are discussed further here: 📖
Antiplatelet therapy: Aspirin or clopidogrel is recommended. A loading dose should be utilized if the patient isn't already on this therapy (note that most patients will already be on an antiplatelet agent). (Bagchi 2025)
Anticoagulation is relatively contraindicated to reduce the risk of hemorrhagic transformation (especially for large strokes). If there are other indications for anticoagulation (e.g., mechanical heart valve), risks and benefits must be carefully considered. Risk factors for hemorrhagic transformation are discussed here: 📖
Statin therapy is usually recommended.

intraparenchymal hemorrhage
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Primary intracranial hemorrhage is rare in post-CTS patients.
Intracranial hemorrhage usually occurs due to hemorrhagic transformation of an ischemic stroke.
Management may include:
- BP should be lowered to a target SBP of 130-150 mm.
- Reversal of anticoagulation.

seizure
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A seizure occurs in ~1% of patients after CABG, mainly within the first two days postoperatively. (Bagchi 2025)
Causes of seizures include:
- Complication of perioperative acute ischemic stroke.
- Withdrawal or under-dosing of chronic antiepileptic agents.
- Withdrawal of alcohol or chronic benzodiazepine therapy.
- Metabolic derangements.
- High-dose tranexamic acid regimens (e.g., >4-6 grams). (Vives 2022)
(Further discussion of seizure: 📖)

early extubation

Most patients can be extubated within <6 hours of ICU arrival (especially routine patients on an ERAS pathway).
Relative exclusion criteria for early extubation may include:
- Preoperative:
  - Pulmonary edema.
  - Intubated.
  - Cardiogenic shock.
  - Sepsis.
- Intraoperative:
  - Deep hypothermic circulatory arrest.
  - Coagulopathy.
  - Severe myocardial dysfunction.
  - Long pump run >4-6 hours.
- Postoperative:
  - Mediastinal bleeding.
  - Hemodynamic instability or the need for an IABP. However, an IABP isn't necessarily a barrier to extubation. Patients with an IABP can often sit up at 30 degrees with the balloon in place. (Kaplan 2024)
  - Respiratory failure or hypoxia.
  - Stroke. (Bojar 2021)

ASV (adaptive-support ventilation)

ASV is an automated ventilator mode that keeps patients comfortable as they awaken from surgery and perform more of their breathing work.
Usual settings following surgery:
- %MV: 100% (default setting)
  - Fever: consider 120%.
  - Asthma: consider 90% (avoid hyperinflation).
- Expiratory trigger sensitivity: 25% (default setting).
- PEEP: 5 cm.
- FiO2: 50%.
- Tube compensation: 100%.
- Rise time: 50 ms. (18580176)
Potential pitfalls of ASV:
- [1] Obese patients may be prone to derecruitment (if usual levels of PEEP are used, such as 5 cm PEEP).
- [2] Tidal volumes may be excessively low in patients with restrictive lung disease. (Titus 2024)
- [3] Rapid-shallow breathing index (RSBI) may be artificially low because the ventilator provides substantial support.

readiness for weaning

✓ Paralysis reversed.
✓ Core temperature >35.5
✓ Hemodynamic stability (none or low-dose pressors).
✓ Good neurological function (following commands).
✓ Chest tube drainage is low.
✓ Review post-operative chest radiograph (no acute pathology that requires intervention).
✓ Review recent chemistries & ABG (acid/base status optimized).
✓ Ventilator settings are reasonably low (e.g., low FiO2 & PEEP; required minute ventilation isn't excessive).

SBT (spontaneous breathing trial)

A traditional spontaneous breathing trial isn't necessarily required (if there aren't concerns regarding extubation).
If a spontaneous breathing trial is desired, the patient can be quickly placed on PSV (pressure-support ventilation) after being awakened. Depending on the level of concern, the spontaneous breathing trial may be continued for a few minutes or up to 30 minutes.
Rising pulmonary artery pressures may be the first hemodynamic abnormality revealing poor tolerance of a weaning trial. (Bojar 2021)
(Further discussion of spontaneous breathing trials: 📖)

post-extubation respiratory support

Extubation to HFNC or BiPAP may be helpful in patients with underlying lung disease.
Nocturnal CPAP or BiPAP benefits patients with OSA, OHS, atelectasis, or other indications.

respiratory deterioration (including dyspnea)
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differential diagnosis may include

Airway:
- Bronchospasm (may be caused by protamine). (Bagchi 2025)
- Vocal cord paralysis (1-2% of patients; injury to recurrent laryngeal nerve; can cause stridor and ineffective cough). (Bojar 2021)
Pleura:
- Pneumothorax (including tension PTX).
- Pleural effusion (~40%).
Lung parenchyma:
- Noncardiogenic: (Bagchi 2025)
  - Pneumonia (~10%).
  - Aspiration pneumonitis.
  - TRALI. 📖
  - Atelectasis (~50%). 📖
- Cardiogenic pulmonary edema.
  - Volume overload.
  - New myocardial ischemia.
  - Valvular dysfunction (new or residual): note that this may cause asymmetric cardiogenic pulmonary edema.
Pulmonary vascular/RV dysfunction:
- Pulmonary embolism.
- Right->Left shunt through a PFO (patent foramen ovale). This may be caused by right ventricular dysfunction or focal tamponade that precipitates elevation of right atrial pressure.
Cardiac:
- Myocardial ischemia (anginal equivalent).
- Tamponade (can manifest with dyspnea, especially in non-intubated patients).
- Arrhythmia.
Neuromuscular:
- Phrenic nerve injury (~15%).
- Critical care neuropathy/myopathy.

investigation may include

Physical examination (including cardiopulmonary POCUS).
Chest radiograph.
ECG (& telemetry).
Selectively: Echocardiography, CT angiography.

epidemiology

Pneumonia is the #1 most common infectious complication of cardiac surgery. (Vives 2022)
The rate of pneumonia might be on the order of ~5-10%. Rates vary due to the vagaries of defining a pneumonia diagnosis.
Risk factors include:
- Smoking.
- COPD.
- Renal insufficiency. (36187899)
- Cardiopulmonary bypass >120 minutes.
- Intraoperative blood transfusion. (Dabbagh 2018)
- Prolonged mechanical ventilation. (33175990)

diagnosis

Diagnosis is challenging, especially in the immediate post-operative context.
Fevers may be caused by cytokine release and wound healing (within <3 days).
The chest radiograph is often abnormal (due to asymmetric pulmonary edema, pleural effusions, pulmonary contusion, and/or atelectasis). (Dabbagh 2018)
- Approach to VAP diagnosis: 📖
- Approach to hospital-acquired pneumonia (non-intubated): 📖

pneumothorax
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epidemiology of post-CT surgery pneumothorax

The risk of pneumothorax after cardiac surgery is ~2%. (Flynn 2020)
Causes of pneumothorax may include:
- Line insertion.
- Opening of the pleura during internal mammary artery dissection.
- Opening of the pleura during off-pump coronary surgery.
- Mechanical ventilation.

management of pneumothorax

Treatment depends on the clinical context.
A small pneumothorax may be observed meticulously, especially in a non-intubated patient.
(Further discussion of pneumothorax: 📖)

post-cardiac injury syndrome (PCIS)
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basics

PCIS is a general term for combinations of pleuropericardial diseases that occur weeks to months after cardiac injury (pleuritis, pericarditis, +/- pneumonitis), often with fever.
PCIS usually occurs about 2-3 weeks after injury. (Murray 2022)

causes & epidemiology of PCIS

s/p Cardiothoracic surgery (aka “postpericardiotomy syndrome”):
- This may affect ~20% of patients.
- Onset is typically 2-3 weeks postoperatively (but can occur within the first week of surgery or several weeks to months later). (Bojar 2021)
- >80% of patients have pleural involvement and develop a pleural effusion. (33175990)
s/p MI (“Dressler syndrome”):
- Affects ~1% of patients with MI. (Sadhu 2023)
- Occurs between one week to three months after MI (most frequently after 1-2 weeks). (ESC 2023, 37622654)
s/p Cardiac trauma (e.g., contusion from blunt trauma).
s/p Pacemaker or ICD implantation.
s/p Ablation for tachyarrhythmias.
s/p PCI (percutaneous coronary intervention).
s/p TAVI (transcatheter valve implantation).

clinical presentation

Two of the following features are usually seen:
- Fever occurs in most patients.
- Pleuritic chest pain (which may reflect pericarditis, pleuritis, or both).
- New pleural effusion.
- Pericardial friction rub.
- Persistent pericardial effusion several weeks after surgery.
Other clinical features:
- Dyspnea (~60% of patients).
- Arthralgias can occur.

ECG

Pericarditis findings may be superimposed over pre-existing abnormalities (e.g., Q-wave MI).
(Further discussion of ECG in pericarditis: 📖).

radiology & POCUS

Pleural effusion (~80%):
- Effusion is usually left-sided or bilateral.
- Effusion is small.
Pericardial effusion (~50%).
Pneumonitis with lung infiltrates may occur in about half of patients.

pleural fluid analysis

Fluid is exudative.
pH is >7.20 and glucose is >60 mg/dL. (Folch 2023)
Initially:
- Pleural fluid may be serosanguinous.
- There may be a neutrophilic predominance.
Over several weeks:
- Serosanguinous transitions into a serous fluid.
- Lymphocyte predominance emerges.

serum labs

Systemic inflammatory markers are usually elevated (e.g., CRP and ESR).
Eosinophilia can be seen in postpericardiotomy syndrome (PCIS following cardiac surgery).

differential diagnosis often includes

Early post-MI pericarditis (usually occurs within four days after transmural MI). 📖
MI (especially re-infarction in patients with prior MI).
Ventricular free wall perforation with hemopericardium (suggested if pericardial effusion >1 cm).
Post-cardiac surgery pleural effusion (discussed further below).
Viral or idiopathic pericarditis.
Pulmonary embolism.
Heart failure.
Pneumonia.

diagnostic approach

Diagnosis of the pericarditis component may be approached similarly to the general criteria for pericarditis. 📖

treatment

Therapeutic drainage:
- Pericardial tamponade is rare, but the pericardial effusion may require drainage.
- Therapeutic thoracentesis may be useful for moderate/large effusions. (Bagchi 2025)
Anti-inflammatory medication:
- High-dose aspirin is useful in post-MI or post-cardiac surgery patients (due to concern that NSAID may increase infarct size). The dose is generally 750-1000 mg PO q8hr for 2 weeks, followed by tapering by 250-500 mg every 2 weeks. (Folch 2023, 37622654)
  - Alternatively, NSAIDs may be helpful in non-MI patients.
- Proton pump inhibitors should be given to prevent gastric ulceration.
- Adjunctive colchicine is generally recommended for three months among patients with pericarditis. (30987913, 37622654) Further discussion of colchicine in pericarditis: 📖
- Steroids are usually reserved for the failure of other medical therapies. Steroids will work rapidly, but there is a high recurrence rate.
The inflammation usually settles within 1-2 weeks. Unfortunately, recurrence is common and may occur delayed (up to ~2 years later).
Pericardial effusion isn't a contraindication to using antithrombotics and/or anticoagulants if these are otherwise indicated. (37622654)

pleural effusion after cardiac surgery (especially post-CABG)
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Early effusions are usually neutrophilic, whereas later effusions are usually lymphocytic. However, it's conceivable that these represent two different stages within the evolution of usual post-CABG effusions. Usually, pleural effusions evolve through various stages:

[1] perioperative effusion (<1 week)

Causes may include diaphragmatic dysfunction, atelectasis, and pleural injury during surgery (with an increased risk following harvesting of the internal mammary artery).
Effusions are usually:
- Small.
- Bloody.
- Left-sided.
- Resolve within two weeks of conservative management. (Folch 2023)

[2] early effusions (1-4 weeks) tend to be bloody & neutrophilic

Timing: Occurs within a month of surgery.
Pleural fluid analysis:
- The fluid is bloody.
- Differential cell count often shows neutrophilia.
- Pleural fluid and/or blood eosinophilia may occur.
- Pleural fluid LDH is high.
Management: Effusions usually respond to 1-2 therapeutic thoracenteses. (Murray 2022)

[3] later effusions (>1 month) tend to be serous & lymphocytic

This often represents a variant of post-cardiac injury syndrome. (23374395, 33175990)
Timing: Usually reach maximal size >1 month after surgery.
Pleural fluid analysis:
- >50% lymphocytosis.
- Relatively low LDH level.
Management:
- Effusions usually respond to 1-2 therapeutic thoracenteses but may be recurrent.
- If there is additional evidence of post-cardiac injury syndrome, then additional treatments for that entity may be helpful (e.g., colchicine).

differential diagnosis

Post-cardiac injury syndrome:
- Features that may suggest PCIS:
  - Patients are more likely to be symptomatic (e.g., fever, chest pain).
  - Pericardial and/or lung parenchymal involvement.
- This is discussed in more detail in the section above.
Empyema (in the perioperative period).
Hemothorax may result from mediastinal bleeding that enters the pleural space. (Dabbagh 2018)
Heart failure (right-sided effusion may be more likely to result from volume overload).
Pulmonary embolism.
Chylothorax. 📖

obstructive lung disease
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evaluation

etCO2 waveform may reveal obstruction.
Clinical wheezing on examination.
Sputum production (may support COPD exacerbation).

management

Bronchodilators.
Adjustment to the ventilator to avoid autoPEEP.
If a true exacerbation of asthma or COPD occurs, these may be managed using usual treatments.
- Treatment of COPD exacerbation: 📖
- Treatment of asthma exacerbation: 📖

phrenic nerve dysfunction
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clinical presentation

Unilateral phrenic nerve paralysis:
- Usually tolerated reasonably well.
- In patients with tenuous respiratory status (e.g., COPD), unilateral phrenic paralysis may impair extubation or contribute to respiratory dysfunction.
Bilateral phrenic nerve paralysis:
- Impairs extubation.
- Leads to paradoxical abdominal breathing.

evaluation

Unilateral phrenic nerve paralysis:
- Causes hemidiaphragm elevation after extubation (usually on the left).
- POCUS may reveal an immobile diaphragm or paradoxical diaphragm movement during inspiration.
Transcutaneous phrenic nerve EMG may help.

management

Initial management is supportive.
Many patients will recover phrenic nerve function (which may take 1-2 years).
An early tracheostomy may be needed. (33175990)
Chronic management may include diaphragmatic plication for persistent unilateral paralysis.

venous thromboembolic disease
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epidemiology

The risk is substantial and similar to other cohorts of critically ill patients:
- DVT incidence is ~15-20%. (7484878)
- PE incidence is ~6-10%.
Risk factors:
- Off-pump surgery.
- Older age.
- History of VTE.
- BMI >30.
- Prolonged immobilization (including intubation).
- Heart failure (including right or left ventricular failure).
- Multiple blood and blood product transfusions.
- Complicated postoperative course (e.g., AKI, infection, neurological complications). (Bojar 2021)
- Heparin-induced thrombocytopenia.

DVT prophylaxis

Mechanical prophylaxis with intermittent pneumatic compression should be applied immediately following surgery.
Chemical DVT prophylaxis may usually be initiated around POD#1 following postoperative hemostasis. However, the risks versus benefits may depend on the individual patient's risks for VTE vs postoperative bleeding. Either unfractionated heparin or low-molecular-weight heparin may be utilized (depending on renal function).

acute kidney injury
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epidemiology: risk of requiring hemodialysis

Roughly ~2-5 % of patients may require dialysis. (Bagchi 2025)
Baseline Cr 2-4 mg/dL: ~15% risk of dialysis.
Baseline Cr >4 mg/dL: ~25% risk of dialysis. (Dabbagh 2018)

risk factors for AKI

Preoperative:
- Preoperative renal dysfunction is the strongest risk factor.
- Preoperative shock, preoperative IABP.
- Urgent/emergent surgery.
- Recent preoperative coronary angiogram (especially <1 day preoperatively).
- Comorbidity:
  - Diabetes (especially requiring insulin).
  - HTN, hyperlipidemia.
  - Reduced LVEF and/or congestive heart failure.
  - COPD.
  - Atherosclerosis, including peripheral artery disease.
- Nephrotoxic medications (especially ACEi/ARB).
- Older age.
Intraoperative:
- Duration of cardiopulmonary bypass & cross-clamp.
- Valve surgery > CABG.
- Hemodilution (hematocrit <21%).
- Hypotension.
- Nephrotoxic medications.
Postoperative:
- Postoperative hemorrhage, transfusion.
- Hemodynamic instability (including sepsis/SIRS, cardiogenic shock, tamponade).
- Myocardial infarction.
- Nephrotoxic medications.
- Need for reoperation. (Dabbagh 2018, Flynn 2020)

evidence-based prevention of postoperative AKI

Dexmedetomidine reduces the risk of AKI (OR 0.66). (37453497)
Vasopressin as a front-line pressor for vasoplegic shock reduces AKI. (VANCS trial 27841822)

investigation of AKI

Laboratory studies:
- Electrolytes (including Ca/Mg/Phos).
- Urinalysis, including sediment analysis.
- Creatine kinase (to exclude rhabdomyolysis, which may reflect extremity compartment syndrome).
Imaging:
- Renal ultrasound or POCUS if needed to exclude obstructive renal failure.
- Echocardiogram to exclude tamponade (may cause renal failure).

management is similar to other AKI in the ICU

Hemodynamic optimization.
- MAP goal >65 mm may be reasonable (possibly higher in patients with chronic hypertension).
- Evaluate for venous congestion and treat it appropriately (e.g., using diuretics, inhaled pulmonary vasodilators, and/or systemic inodilators such as milrinone to improve right ventricular function). However, also beware that cardiac tamponade can present with AKI!
- Further discussion of general hemodynamic optimization after surgery is above: ⚡️
Medication management:
- Discontinue & avoid nephrotoxins. 📖
- Dose-adjust renally cleared medications.
Potassium:
- Caution with potassium supplementation in severe AKI.
- Treat hyperkalemia if present.
Phosphate:
- Renal diet in severe AKI.
- Consider phosphate binder if phosphate >6 mg/dL.
  - In hypocalcemia: calcium carbonate or calcium acetate (~600 or ~667 mg TID with meals).
  - Otherwise, sevelamer 800 mg TID should be taken with meals.
Acidosis management:
- Consider bicarbonate for mild uremic metabolic acidosis. 📖
Hemodialysis if indicated.

questions & discussion
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To keep this page small and fast, questions & discussion about this post can be found on another page here.

Guide to emoji hyperlinks

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39141254 Tolj V, Adegbenro T, Brovman EY. Optimizing Pain Management in Cardiac Surgery: A Review of Analgesic Adjuvants. Curr Pain Headache Rep. 2024 Dec;28(12):1249-1253. doi: 10.1007/s11916-024-01304-9 [PubMed]

Books

Dabbagh, A., Esmailian, F., & Aranki, S. (2018). Postoperative critical care for adult cardiac surgical patients. Springer.
Flynn, B., Ivascu, N. S., Moitra, V. K., & Gaffney, A. (2020). Cardiothoracic critical care. Oxford University Press.
Bojar, R. M. (2021). Manual of Perioperative Care in Adult Cardiac Surgery. John Wiley & Sons.
Sundt, T. M., Cameron, D. E., & Lee, M. E. (2022). Near misses in cardiac surgery. Springer Nature.
Vives, M., & Hernandez, A. (2022). Cardiac anesthesia and postoperative care in the 21st century. Springer Nature.
Kaplan, J. A. (2023). Kaplan’s cardiac anesthesia. Elsevier.
Bagchi, A., MDudzinski, D., Ludmir, J., Nikolic, I., & Shelton, K. T. (2025). Massachusetts General Hospital Manual of Cardiovascular Critical Care. Lippincott Williams & Wilkins.

CONTENTS

general postoperative management

hemodynamic pertubations

arrhythmias

other cardiovascular problems

endocrine

gastroenterology

hematology

ID

neurology

pulmonary

renal

general postoperative management(back to contents)

general postoperative management

initial evaluation in ICU

general postoperative objectives

postoperative chest radiograph(back to contents)

postoperative chest radiograph

ETT 📖

IABP 📖

right heart catheter

epicardial pacing leads

mediastinal drains

mediastinal width

postoperative concerns after SAVR(back to contents)

postoperative concerns after SAVR

impaired diastolic function (e.g., normal EF with a small chamber)

paravalvular leak

LV outflow tract obstruction (LVOTO)

postoperative concerns after TAVR(back to contents)

postoperative concerns after TAVR

heart block

acute hemodynamic deterioration

differential diagnosis

evaluation

bleeding & vascular complications

hemorrhage

other vascular complications

stroke

acute kidney injury

postoperative concerns after mitral valve surgery(back to contents)

postoperative concerns after mitral valve surgery

pulmonary HTN & RV dysfunction

surgery for mitral regurgitation

LV outflow tract obstruction (LVOTO)

hemodynamic parameters & rough targets(back to contents)

hemodynamic parameters & rough targets

perfusion targets

MAP ~60-90 mm; SBP ~100-140 mm

CVP <~12 mm

PAD (or PCWP)

heart rate

cardiovascular deterioration, including low CO syndrome(back to contents)

cardiovascular deterioration, including low CO syndrome

differential diagnosis of cardiovascular deterioration

reduced preload

obstructive cardiovascular physiology

excessive vasodilation

LV failure

RV failure

valvular dysfunction

arrhythmia

evaluation

bedside investigations

laboratory studies

advanced testing

management: general hemodynamic optimization

treat any underlying etiologies, e.g.:

volume management

management of SVR & MAP

management of systolic LV failure

management of insufficient heart rate

diagnose & treat RV dysfunction

mechanical cardiac support

vasoplegic syndrome(back to contents)

vasoplegic syndrome

epidemiology

definition

differential diagnosis

management

general postoperative management
(back to contents)

postoperative chest radiograph
(back to contents)

postoperative concerns after SAVR
(back to contents)

**impaired diastolic function (e.g., normal EF with a small chamber)**

postoperative concerns after TAVR
(back to contents)

postoperative concerns after mitral valve surgery
(back to contents)

hemodynamic parameters & rough targets
(back to contents)

cardiovascular deterioration, including low CO syndrome
(back to contents)

vasoplegic syndrome
(back to contents)

tamponade & pericardial effusion
(back to contents)

hypertension
(back to contents)

postoperative atrial fibrillation & flutter: prevention
(back to contents)

postoperative atrial fibrillation & flutter: management
(back to contents)

postoperative monomorphic VT (or polymorphic VT due to ischemia)
(back to contents)

bradyarrhythmias
(back to contents)

atrial electrography (AEG)
(back to contents)

epicardial pacing
(back to contents)