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Complications of Cardiac surgery

Moderator: Dr. Moaath Asmady


Presenter: Dr. Tareq Al-Qasas

Cardiac complications
Low

cardiac output
Cardiac arrest
Arrhythmias
MI
Coronary artery spasm
Cardiac Tamponade

Respiratory complications

Atelectasis
Bronchospasm
Phrenic nerve injury
Prolonged respiratory insufficiency
ARDS
Pneumothorax
Pleural effusion
PE

Blood and clotting complications


Bleeding
Fibrinolysis
DIC
DVT

Renal complications
Acute

Renal Failure

Infectious complications
Pneumonia
Wound

infection
Mediastinitis
Catheter sepsis

GI complications
Ileus
Upper

GI bleeding
Intestinal ischemia
Acute Cholecystitis
Acute Pancreatitis
Acute Hepatic Failure
Nausea, Dysphagia, Hiccups

Neurological complications
Stroke
Neurobehavioral

disturbances
Peripheral Nerve Injury

Low Cardiac Output


Requirement

of IABP
Significant dose of inotropic agent for more than
30 min
Incidence 10-20%

Causes

Preop ventricular dysfunction


Inadequate myocardial protection
Incomplete myocardial revascularization
MI
Coronary or graft spasm
Arrythmias
Outflow obstruction
Inadequate fluids
Cardiac Tamponade
Sepsis, anaphylaxis, adrenal insufficiency, PEEP, etc.

Prediction of low cardiac output


preoperatively
Cath
Echo
Determination

of LVEF

Predictors of low cardiac output

Left ventricular ejection fraction less than 20% (27%)


Repeat operation (25%)
Emergency operation (25%)
Female gender (16%)
Diabetes (13%)
Age older than 70 years (13%)
Left main coronary artery stenosis (12%)
Recent myocardial infarction (16%)
Triple-vessel disease (10%)
RaoV.IvanovJ.WeiselRD,J.thorac.cardiovasc.surg.1996112,38-51

Prevention of low cardiac output


Venting

the left ventricle


Combined ante grade and retrograde cardioplegia
Lower perfusion temperatures
Femoral artery catheterization
Intra Aortic Balloon Pump

Management of low cardiac output


syndrome

Look for noncardiac correctable causes


Treat ischemia or spasm (NTG, Nifedipine, Diltiazim)
Optimize preload (PCWP 18-20 mm Hg)
Optimize heart rate (90-100 bpm)
Control arrhythmias
Correct anemia (if Hct<26)
CO, CI, SVR assessed and optimized
Intra-aortic balloon pump (IABP)
Ventricular assisting device (VAD)

Hemodynamic problems
BP

PCW

CO

SVR

Plan

Volume

Venodilator or diuretic

Inotrope

Vasodilator

Inotrope/Vasodilator/IABP

-agent

Right ventricular failure


RCA disease
RV infarction
Pulmonary

hypertension
Inadvertent trauma to RCA
RV hypoperfusion
Intrinsic pulmonary disease, ARDS, PE

Treatment of right ventricular failure

Optimize preload (CVP 18-20 mm Hg)


Ensure AV conduction
Ensure systemic perfusion (vasoactive substances, IABP)
Lower PVR, improve RV contractility
Correct hypothermia, hypoxia, hypercarbia, acidosis
Vasodilator inotropes (milrinone, dobutamine, low dose epinephrine)
Pulmonary vasodilators (nesiritide, NO, PGI2, adenosine, PGE1,
endothelin antagonist)

Optimize LV function
RVAD

Inotropic Agents commonly used

Dobutamine
Dopamine
Ephedrine
Epinephrine
Isoproterenol (rarely used)
Milrinone
Norepinephrine
Phenylephrine

Perioperative nesiritide administration (2 gkg1 load,


followed by 0.01 gkg1min1 for a maximum of 24 h)
resulted in a statistically significant median increase in CO
of 35%. In conclusion, nesiritide was associated with
increased CO in patients with low CO syndromes
undergoing cardiac surgery, when other measures failed
Journal of Anesthesia
Volume 20, Number 4 / November, 2006
George R.G, Roman S, Hassan R, Kamal K, Michael R

Management of low cardiac output

Intra-aortic balloon pump


Provides

physiologic assistance to the heart


Decreases myocardial oxygen demand and
improves coronary blood supply

Mechanism of action
Rapid

inflation just after aortic valve is closed


allowing better coronary perfusion
Rapid deflation just before ventricular systole to
reduce impedance to LV ejection
Thus it reduces time-tension index and increases
diastolic pressure- time index improving the
oxygen supply-demand ratio

Indications

Ischemia refractory to medical treatment


Prophylactic in patients with critical coronary artery
disease or severe LV dysfunction
High risk patients ongoing off-pump surgery
Cardiogenic shock or mechanical complications after MI
Post op low cardiac syndrome not responsive to moderate
inotropes
Post op MI
Acute deterioration of LV function

Contraindications
Aortic

insufficiency
Aortic dissection
Severe aortic and peripheral vascular
arteriosclerosis

Insertion
Percutaneous
Surgical

Complications

Limb ischemia (5-18%)


Insertion site hemorrhage (2-4%)
Infection (1-2%)
Aortic or iliac perforation (1-2%)
Aortic dissection (1%)
Renal artery embolism or thrombosis (1%)
Mesenteric infarction (1%)
Spinal cord injury (0.5-1%)
Gas embolization/rupture (0.5%)
CVA (0.5%)

Causes of bleeding

Could be classified into surgical or medical


Surgical:
Inadequate Homeostasis
Site of aortic or venous canulea
Slipped clip or ligature
Side branches of arterial or venous conduits
Substernal soft tissues
Sternal suture sites
Bone marrow
Periosteum
Raw surfaces caused by previous surgery , radiation, or pericarditis

Causes of bleeding

Medical causes:

Platelet depletion
Platelet dysfunction
Clotting Factor Deficiency
Residual Heparin Effect
Excessive Protamine Administration
Hypothermia
Increased Fibrinolytic Activity
Consumptive Coagulopathy
? Genetic factors

Genetic factors

Seven genetic polymorphisms associated with bleeding after cardiac surgery. Genetic
factors appear primarily independent of, and explain at least as much variation in
bleeding as clinical covariates; combining genetic and clinical factors double our
ability to predict bleeding after cardiac surgery. Accounting for genotype may be
necessary when stratifying risk of bleeding after cardiac surgery
GPIaIIa-52C>T and 807C>T,
GPIb alpha 524C>T,
tissue factor-603A>G,
prothrombin 20210G>A,
tissue factor pathway inhibitor-399C>T, and
angiotensin converting enzyme (ACE) deletion/insertion
PEGASUS investigative team
Department of Anesthesiology, Duke University Medical Center, Durham

Prevention of bleeding
Assessment

of bleeding tendency preoperatively


Cessation of medications
Antifibrinolytic therapy
Autologous blood transfusion
Platelet rich plasmapheresis
Meticulous surgical technique
CPB consideration

Cessation of medications

Warfarin: 4 days
Heparin: no need to be stopped
LMWH: 12 hours
Aspirin: 3 days
Clopidogril(Plavix): 5-7 days
Ticlopidine(Ticlid): 7 days
Tirofiban: 4 hours
Abciximab: 12-24 hours
Thrombolytic therapy: 12-24 hours

Antifibrinolytic therapy
Aprotinin
-aminocaproic

acid
Tranexamic acid

Autologous blood withdrawal


Protects

platelets against CPB


Preserves red cell mass and reduces transfusion
requirements
Role in reducing bleeding still controversial
Schonberger JP et al, Ann Thorac Cardiovasc Surg 1994;107:1210-4
Ramnath AN et al, J Thorac Cardiovasc Surg 2003; 125:1432-7

Platelet rich plasmapheresis

Withdrawal of platelet-rich plasma at the beginning


Readministration
Improves homeostasis
Reduces blood loss
Expensive
Time consuming
More applicable in Redo operations
Shore-Lesserson L, Reich DL, Anesth Anal 1995;81:229-35
Christenson JT, Reuse J, Ann Thorac Surg 1996;62:1373-9

CPB considerations
Heparin-coated

circuits
Retrograde autologous priming
Avoidance of cardiotomy suction
Balachandran S, Cross MH, Ann Thorac Surg 2002;73:1912-8
Johnell M, Larrson R, J Thorac Cardiovasc Surg 2002;124:321-32

Assessment of bleeding
Documentation

of amount of blood in drains


Type of blood in drains
Hemodynamic values (Swan-Ganz, TEE)
Potential causative factors (coagulation profile)
Suspicion of undrained blood (CXR, breath
sounds, peak inspiratory pressures)

Management of bleeding

Ensure chest tube patency


Warming to normothermia
10 cm PEEP
Control HTN (nitroprusside, -blockers)
Control shivering (meperidine, pancuronium)
Control agitation (propofol, midazolam, morphine)
Coagulation profile
Blood and blood components
Drugs
TEE
Early exploration if surgical causes are suspected

Blood and its products


PRBC

if Hct <26
Platelets 1 unit/10 kg
FFP 2-4 units
Cryoprecipitate 1 unit/10 kg

Drugs
Protamine

25 units once or twice


Aprotinin 2 million units
Desmopressin 0.3-0.4 g/kg
Calcium chloride 1 gm IV
Factor VIIa

Aprotinin
Useful

only when given postoperatively

Desmopressin
Desmopressin

is beneficial for surgical patients at


high risk for excessive bleeding
Patients who received desmopressin lost 40% less
blood compared with those who received placebo
and required less postoperative transfusion: 50%
fewer red blood cells, 95% fewer platelets, and
87% less fresh-frozen plasma
Despotis GJ et al. Lancet 1999 354 106-110.

Factor VIIa

No thromboembolic complications were observed in patients


receiving FVIIa. Blood loss and transfusion requirements were
significantly reduced in the period after the administration of FVIIa.
However, in the 24-hr period after FVIIa administration, blood loss
and transfusion of packed red blood cells and fresh frozen plasma
were not different after administration of FVIIa. Mortality and 6month survival rates were not different.
CONCLUSIONS: When used as a last resort, FVIIa was safe but not
incrementally efficacious over conventional haemostatic therapy.
Spies C et al,
Department of Anesthesiology and Intensive Care Medicine, St. Mary's Medical Center, San
Francisco, CA, USA.

Indications for exploration


More

than 400 ml/hr for 1 hour( 200 ml/m2)


More than 300 ml/hour for 2-3 hours(150
ml/m2/hour)
More than 200 ml/hour for 4 hours(100
ml/m2/hour)

Management of bleeding

Cardiac Tamponade
Should be suspected when the patient has hemodynamic
compromise with rising filling pressures
Suspicion increases if:
Sudden cessation of significant mediastinal bleeding
low cardiac output and hypotension with respiratory variation and narrow
pulse pressure
Widened mediastinum or displaced cardiac right shadow
Equalization of intracardiac pressures
Tachycardia
Arrythmias, decreased ECG voltage, EMD

Cardiac tamponade
Diagnosis

is confirmed by echo
Management is by early exploration