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%)

Rao V. Ivanov J. Weisel RD, J. thorac. cardiovasc. surg.1996 112, 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

N ↑ N ↑ Venodilator or diuretic

↓ ↑ ↓ ↑ Inotrope

↑ ↑ ↓ ↑ Vasodilator

↑ ↓ ↑ ↓ ↑ Inotrope/Vasodilator/IABP

↓ N N↑ ↓ α-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 µg·kg−1 load, followed by 0.01 µg·kg−1·min−1 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 ε-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;81:229-35Christenson 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, ß-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 μg/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 6-month 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