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191
Case Study Number 2
A 63-year-old male with symptomatic severe aortic stenosis underwent aortic
valve replacement with a 23 mm pericardial valve. His postoperative course
was complicated by asystolic cardiac arrest due to complete heart block
requiring temporary pacing, agitation, confusion altered mental status, and
aspiration requiring re- intubation. On postoperative day 7, the patient was
started on unfractioned heparin for atrial fi brillation.
On postoperative day 9, the patient platelet count dropped to 45,000 × 10
3
per mm
3
, the patient developed tachypnea and hypoxemia. The PF4/IgG assay
was sent and came back (with a value of 2. 48 anti-heparin/PF4 antibody OD
value). Bivalirudin was started. The clinical presentation included RUL/LLL
PE, left gastrocnemius DVT, and seizures due to embolic events confi rmed by
tiny punctate infarcts on MRI in the right frontal lobe. Platelet count recov-
ered over 100,000 on postoperative day. Coumadin was started and over-
lapped with intravenous bivalirudin until the INR was therapeutic. The patient
was discharged on postoperative day 23 and continued on Coumadin for 6
months.
Day of hospialization
Platelet count (1,000/mcL)
1st ICU
Preop
POD 1
POD 2
POD 3
POD 4
POD 5
POD 6
POD 7
POD 8
POD 9
POD 10
POD 11
POD 12
POD 13
POD 14
POD 15
POD 16
POD 17
POD 18
POD 19
POD 21
POD 20
POD 22
Disch.
180
160
140
120
100
80
60
40
20
0
IV Heparin
DC Bival
Coumadin started
PF4 2.48 HIT +
DC Heparin
Case Study #2
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6.8.7 Discussion
These two cases illustrate the clinical course of HIT. Both patients had recent expo-
sure to unfractionated heparin with drop in platelet count and the presence of throm-
boembolic complications. In case #1, the clinical picture was so overwhelming for
the diagnosis of HIT (sudden drop in platelets count, unexplained symptoms, skin
necrosis) that we decided to treat the patient accordingly even though the anti-PF4-
heparin Ab level was a borderline value.
These two patients summarizes that HIT is associated with high morbidity and
prolonged hospital stay. The fi nancial implications of HIT are signifi cant.
6.8.8 Future Directions
Unfractionated heparin will continue to be used in cardiac surgical patients because
it is safe for cardiopulmonary bypass. Future advances may be directed toward the
treatment of HIT. The introduction of oral direct thrombin inhibitors may be used as
an alternative to the intravenous and subcutaneous counterparts. In addition they
can be continued to the outpatient setting without the need for Coumadin combined
with intravenous therapies. Such an strategy undoubtedly will result in reduced hos-
pital stay and cost.
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Pouplard C, May MA, Iochmann S et al (1999) Antibodies to platelet factor 4–heparin after car-
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penia. Blood 67:27–30
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bocytopenia/thrombosis are specifi c for platelet factor 4 complexed with heparin or bound to
endothelial cells. J Clin Invest 93:81–88
Warkentin TE (1996) Heparin-induced thrombocytopenia: IgG-mediated platelet activation, plate-
let microparticle generation, and altered procoagulant/anticoagulant balance in the pathogene-
sis of thrombosis and venous limb gangrene complicating heparin-induced thrombocytopenia.
Transfus Med Rev 10:249–258
Warkentin TE (1998) Limitations of conventional options for heparin induced thrombocytopenia.
Semin Hematol 35(4 suppl 5):9–16
Warkentin TE (2003) Heparin-induced thrombocytopenia: pathogenesis & management. Br J
Haematol 121:535–555
Warkentin TE (2004) Clinical picture of heparin-induced thrombocytopenia. In: Warkentin TE,
Greinacher A (eds) Heparin- induced thrombocytopenia, 3rd edn. Marcel Dekker, New York,
pp 53–106
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Warkentin TE, Greinacher A (2004) Heparin-induced thrombocytopenia: recognition, treatment,
and prevention – the 7th ACCP conference on antithrombotic & thrombolytic therapy. Chest
126:311S–337S
Warkentin TE, Heddle NM (March 2003) Laboratory diagnosis of immune heparin- induced
thrombocytopenia. Curr Hematol Rep 2(2):148–157
Warkentin TE, Kelton JG (1996) A 14-year study of heparin-induced thrombocytopenia. Am J
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Warkentin TE, Sigouin CS (2002) Gender and risk of immune heparin-induced thrombocytopenia.
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Warkentin TE, Hayward CP, Smith CA et al (1992) Determinants of donor platelet variability
when testing for heparin-induced thrombocytopenia. J Lab Clin Med 120:371–379
Warkentin TE, Levine MN, Hirsh J et al (1995) Heparin-induced thrombocytopenia in patients
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332:1330–1335
Warkentin TE, Sheppard JA, Horsewood P et al (2000) Impact of the patient population on the risk
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6.8.9 Appendix A.1 Agents Used for Treatment of HIT
Agents Dosage
Danaproid IV bolus (1,500 U if patient is 60 Kg, 2,250 U if 60–75 kg, 3,000 U if
75–90 Kg, 3,750 U if >90 Kg)
Intravenous infusion 400 U per hour for 4 h, 300 U per hour for 4 h,
150–200 U per hour
Monitoring
Adjust to anti-factor Xa activity of 0.5–0.8 U per milliliter
Argatroban IV infusion 2.0 μg per kilogram; decrease in patients with liver disease
or critical illness (to 0.5–1.2 μg per kilogram)
Monitoring
Adjust to maintain activated partial thromboplastin time at 1.5–3.0 times
baseline value
Bivalirudin 0.15–2.0 mg per kg/h
Monitoring
Adjust to maintain activated partial thromboplastin time at 1.5–2.5 times
baseline value
Fondaparinux 5.0 mg SQ qday for patients, 50 kg; 7.5 mg for 50–100 kg; 10 mg for
patients >100 kg
Monitoring
None
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A. Dabbagh et al. (eds.), Postoperative Critical Care for Cardiac Surgical Patients,
DOI 10.1007/978-3-642-40418-4_7, © Springer-Verlag Berlin Heidelberg 2014
Abstract
The essential principle in post-cardiac surgical care is ensuring optimal hemody-
namic preservation and tissue perfusion through the utilization of continuous
hemodynamic monitoring, adequate volume repletion, and, if necessary, use of
inotropic agents and/or pressors. Cardiopulmonary resuscitation (CPR) for
M. Foroughi , MD (*)
Cardiovascular Research Center , Shahid Beheshti University
of Medical Sciences , Tehran , Iran
e-mail: mahnoosh.foroughi@gmail.com, m_foroughi@sbmu.ac.ir
A. H. Conte , MD, MBA
Perioperative Transesophageal Echocardiography Education,
Division of Cardiothoracic Anesthesiology, Department of Anesthesiology ,
Cedars-Sinai Medical Center , Los Angeles , CA , USA
e-mail: antonio.conte@cshs.org
7
Cardiovascular Complications
and Management After
Cardiac Surgery
Mahnoosh Foroughi and Antonio Hernandez Conte
Contents
7.1 Cardiac Monitoring ......................................................................................................... 198
7.1.1 Cardiovascular Effects of Common Inotropic Agents ........................................ 199
7.2 Cardiac Complications .................................................................................................... 199
7.2.1 Postoperative Myocardial Ischemia .................................................................... 199
7.2.2 Hemodynamic Instability .................................................................................... 200
7.2.3 Arrhythmias ........................................................................................................ 202
7.3 Vasoplegic Syndrome ...................................................................................................... 204
7.4 Postoperative Cardiac Tamponade (POCT) .................................................................... 204
7.5 CPR After Cardiac Surgery............................................................................................. 205
7.6 Assist Devices ................................................................................................................. 207
7.6.1 Intra-Aortic Balloon Pump (IABP) ..................................................................... 207
7.6.2 Ventricular Assist Device (VAD) ........................................................................ 208
7.6.3 Extracorporeal Membrane Oxygenation (ECMO) .............................................. 209
References ................................................................................................................................ 210
https://t.me/med1917
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cardiac arrest after cardiac surgery is different from cardiac arrest in other set-
tings as its causes are usually reversible with associated improved outcomes.
Due to aging of the cardiac surgical population and broader application of
interventional cardiologic interventions before admission for cardiac surgery, the
profi le of patients has changed. Cardiac surgical patients in the twenty-fi rst cen-
tury are older and sicker, possess diminished physiologic reserve, manifest
decreased ventricular function, are referred for more complex procedures, and
are at high risk for postoperative major cardiac complications in comparison
with other patient populations. The main insult sustained by the patient is related
to inadequate myocardial contraction that results in a low cardiac output syn-
drome. Inability to wean from cardiopulmonary bypass created more emphasis
in evaluating means of more prolonged supportive measures. Innovative tech-
niques for circulatory support devices have developed, and different types are
now available. Initially intra-aortic balloon pumps (IABP) and centrifugal pumps
were developed, whereas now rapidly evolving technical changes have led to
new and improved pneumatic and electrically driven internal assist devices.
These devices are being increasingly inserted in an effort to provide supportive
assistance to one or both ventricles with increased safety and durability.
7.1 Cardiac Monitoring
Upon arrival to the ICU, the post-cardiac surgical patient requires intense adequate
hemodynamic monitoring; this is accomplished via continuous ECG, arterial blood
pressure measurement via arterial catheter, frequent arterial blood gas sampling,
central venous pressure (CVP) measurement via central venous catheter, pulse
oximetry, and evaluation of chest tube drainage. The use of a pulmonary artery
catheter is validated in pulmonary hypertension, severe low cardiac output, and
partition of right and left ventricular failure; however, its use is associated with
multiple risks and higher morbidity and mortality when inappropriately utilized.
The main aim in post-cardiac surgical care is to maintain optimal hemodynamics
with resultant normal tissue perfusion achieved by suffi cient intravascular volume and
cardiac output. Although, during CPB there is increased weight gain due to water
retention, it is distributed to the extravascular component. However, the hypovolemic
condition postoperatively is common. CVP is considered an approximate indicator of
preload status. It is recommended to keep CVP >10 mmHg by volume repletion; by the
same respect, a CVP >20 mmHg may warrant diuresis. Before volume administration,
hemodynamic response to increasing preload can be assessed by passive leg rising.
After cardiac surgery reduced myocardial function may be due to inadequate
valve repair or insuffi cient revascularization, ischemic reperfusion injury, myocar-
dial edema, reduced preload, and increased afterload. The adequacy of cardiac per-
formance during the postoperative period in the ICU is assessed by cardiac index,
arterial blood pressure, pedal pulses, skin temperature, mixed venous oxygen satu-
ration level, urinary volume, and metabolic acidosis. Possible indicators of insuffi -
cient cardiac performance are:
M. Foroughi and A.H. Conte
https://t.me/med1917
199
Mean arterial pressure < 60 mmHg
Serum lactate > 2 mmol / L
Urinary output < 0 . 5 mL / h
Svo
2
< 60 % with Sao
2
> 95 %
Central-mixed venous oxygen saturation (SVO
2
) is a very accurate indicator of
tissue perfusion, as it demonstrates the relationship between oxygen supply (deter-
mined by cardiac output) and demand (metabolic state).
Some causes of low cardiac output after cardiac surgery are evaluated by elec-
trocardiogram, chest X-ray, hemodynamic data, and echocardiography. ECG
changes may be suggestive of myocardial ischemia or infarction, signifi cant chest
tube drainage, and blood collection, or signs of tamponade may be noted through
chest X-ray, and echocardiography can delineate new ventricular wall motion
abnormalities, decreased ejection fraction (EF), and new or residual valvular
pathology (Wasir et al. 2003 ; Joshi et al. 2005 ; Overgaard and Džavík 2008 ).
7.1.1 Cardiovascular Effects of Common Inotropic Agents
The primary treatment for low cardiac output states has been pharmacologic inter-
ventions. Catecholamines exert their cardiovascular effects through α-, β
1−
, β
2−
, and
dopaminergic receptors. α-receptor activation causes arterial vascular smooth muscle
contraction and rising in systemic vascular resistance (SVR). β
1
-receptor stimulation
in myocardium causes increased contractility and conduction velocity. β
2
-receptor
activation causes vascular smooth muscle relaxation and reduction in SVR.
Dopaminergic receptor in kidney and splanchnic circulation causes vasodilation.
Epinephrine in low dose acts in β
1
-receptors and in high dose acts in α-receptors.
Norepinephrine is a potent α-receptor agonist, enhancing SVR via vasoconstriction.
Phenylephrine as α-receptor agonist is used in bolus setting to correct hypotension.
Pharmacologic support in patients with low cardiac output may be obligatory in
the postoperative period. However, before starting inotropes, improvement of preload
status and SVR reduction must be considered because cardiac output is a function of
myocardial contractility and hemodynamic conditions (afterload and preload).
7.2 Cardiac Complications
7.2.1 Postoperative Myocardial Ischemia
While a large majority of cardiothoracic surgery is performed in order to optimize
vascular supply to the heart via coronary artery bypass grafting, postoperative myo-
cardial ischemia (PMI) and associated myocardial infarct (MI) continue to remain a
signifi cant complication in the postoperative setting. The Society of Thoracic
Surgeons (STS) maintains a clinical database for every cardiothoracic surgical pro-
cedure performed; the STS has defi ned perioperative ischemia as the occurrence of
at least one of the following markers: (1) electrocardiographic changes consistent
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with ischemia, (2) elevation of serum markers (i.e., troponin), and (3) reduced
systolic ejection fraction. The incidence of PMI in the STS database is 1 %.
7.2.1.1 Diagnosis
The diagnosis of postoperative myocardial ischemia is based upon detection of the
aforementioned markers. The most common laboratory tool for assessment of PMI
is measurement of troponin I or cardiac troponin. Patients who manifested elevated
preoperative levels of troponin may not necessarily imply PMI in the postoperative
period. In addition, patients who underwent coronary artery bypass grafting (CABG)
with the use of cardiopulmonary bypass (CPB) were more likely to have elevated
levels of troponin compared to patients who were “off-pump”; troponin levels were
more apt to remain within normal limits if CPB during CABG is not utilized.
Elevation of the MB fraction of creatine kinase may also be measured and may be
indicative of PMI. Since the majority of PMI may occur while a postsurgical patient
is still intubated, symptoms associated with angina may not be elicited; therefore,
electrocardiographic detection with follow-up laboratory assessment is paramount.
The type of cardiac surgery performed may allow the clinician to more accu-
rately assess the etiology for PMI. In cases where coronary artery bypass grafting
has been conducted, patients may be prone to closure of newly created vascular
coronary conduits, as well as residual myocardial injury secondary to poor myocar-
dial protection. Patients having undergone valve repair or replacement, especially
aortic valve replacement, as well as aortic root surgery may be prone to anatomic
disturbances in coronary blood fl ow originating at the coronary ostia. Diagnosis
may require invasive cardiac catheterization to rule out reocclusion or new occlu-
sion of coronary ostia or their tributaries.
7.2.1.2 Management
Treatment of coronary myocardial ischemia is targeted at maneuvers to improve or
restore coronary perfusion and resultant myocardial perfusion. In the absence of
arterial hypotension, the initiation of intravenous venodilators (i.e., nitroglycerin)
and arterial vasodilators (sodium nitroprusside) may yield signifi cant improvement.
In addition, the administration of calcium channel blockers (nifedipine, nicardipine)
may ameliorate vasospasm in cardiac arterial blood vessels. The need to augment
oxygen-carrying capacity may also require the administration of red blood cell
transfusion. Patients not responding to restoration of arterial diastolic pressure con-
comitant with use of preferential vasodilators may necessitate further evaluation
with cardiac catheterization or invasive assessment with a pulmonary artery cathe-
ter. Efforts should be made to initiate the appropriate treatment intervention as soon
as possible.
7.2.2 Hemodynamic Instability
Patients undergoing cardiac surgery undergo signifi cant alterations in temperature,
circulating blood volume, initiation of cardiopulmonary bypass, myocardial
M. Foroughi and A.H. Conte
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