COMPLICATIONS OFCARDIOTHORACIC
SURGERY
Jacqueline Palmer-Powell, RNNurse Educator/CNS
Complications Commonly Resulting From Cardio-Thoracic
Surgery
CVA
CVA Devastating complication that
results in lasting deficits of death. Other neurological complications
which are more subtle occur with more frequency.
Incidence -CABG with CPB: 2-5% -Valve Surgery: 5-10%
Risk Factors
Prior history of stroke, HTN, DM Carotid disease, carotid bruit Advanced age Atrial Fib
Diagnosis & Treatment
CT Scan demonstrates cerebral infarct within 1-2 days
No treatment exist other than palliative
Early rehabilitation Family counseling
Hypotension
Definition: Systolic BP<100 Cause: hypovolemia, excessive
vasodilation, sepsis, elevated or decreased HR
Treatment: identify cause!, volume replacement, use of IV drips
Bleeding
Contributing Factors in Bleeding Complication Pre-op Post-op Acute MI treated with - Vigorous
chest thrombolytics (failed) tube stripping
Aspirin - Hypertension IIBIIIA Platelet - Heparin Co-morbid states (uremia, liver disease)
What Constitutes Excessive Bleeding?
Chest Tube Drainage: - >500cc/hr in first hour - >400cc/hr during first 2 hours - >300cc/hr during first 3 hours - >200cc/hr during first 6 hours
Basis of Coagulation
Coagulation Cascade with the help of endothelium & platelets is the body’s defense to minimize blood loss.
A vascular insults stimulates formation of platelet plug thru platelet activation, adhesion & aggregation. The plug is then stabilized thru clotting cascade to a fibrin clot
Clotting Cascade
Effect of CPB on Coagulation
Major CPB induced coagulopathy results from platelet activation, dysfunction & destruction.
Structural damage to platelets & RBC’s can occur thru shearing forces & turbulence in CPB pump, circuits & suction devices
Preventing Bleeding Before Surgery
Complete History - Questions about previous surgery,
family history, bruising, heavy menses
- medication history (Prescribed, OTC & herbal)
Physical Exam Blood Work
Pre-op Bleeding Prevention Identification of patient with co-morbid
states that may contribute to bleeding: - Uremia: Causes platelet dysfunction
thru impaired VWF interaction with platelets.
- Acute liver dysfunction: may result in factor deficiency as a results of impaired factor production & may lead to DIC
Drugs Which Affect Bleeding
Aspirin NSAIDS IIBIIIA Platelet Inhibitors Coumadin Thrombolytics Heparin
Prevention & Treatment of Bleeding in OR Thorough search for bleeding before
chest closure including careful inspection of skin, sternum, suture sites
Autotransfusion: pre-op blood donation (self-directed) with re-infusion after CPB
Cell-saver-blood drained from chest tubes in OR collected thru special filters & reinfused after surgery
DIC Diagnosis: Increased products of fibrin
degradation (d-dimer), thrombocytopenia & prolongation of both PT & PTT
Treatment: Replacement with PRBC, FFP & platelets. If fibrinogen level low, replacement with cryoprecipitate is preferable. Drugs (Amikar, Aprotinin) may be useful in treating DIC. High mortality!
Drugs Used To Treat Bleeding Protamine SO4: Protein derived from
salmon sperm. Used to neutralize effects of heparin
DDAVP: Analog of vasopressin may be used when a patient continues to bleed despite normal coagulation profile & platelet counts
Antifubrinolytics: Help to achieve homeostasis in patients with excessive fibrinolysis
Blood Products
Depending on patient presentation, history & lab results the bleeding may require infusion(s) of PRBC, platelets, FFP, &/or cryoprecipitate to control the bleeding & prevent hemodynamic instability
Re-Op for Bleeding Chest Exploration
<3% of patients require re-op to search for bleeding
Bleeding causing tamponade or severe hypotension requires immediate re-op
Coagulopathy must be distinguished from anatomic cause
Low Cardiac Output Syndrome
Signs & Symptoms of LCOS Results directly from inadequate tissue
perfusion & increased sympathetic activity.
Cool, clammy skin with slow capillary refill
Oliguria Mental status changes Metabolic acidosis Fall in SVO2
Causes of LCOS Any pre-op condition - Post –op conditions
that that causes impairment cause myocardial
dysfunction: of preload, after load &/or contractility - hypothermia Events in OR - acidosis Arrhythmias - hypercarbia Inadequate preload or - volume overload elevated intrathoracic - increased afterload pressure
Treatment of LCOS
Heart rate manipulation Preload Afterload Myocardial Contractility
SHOCK
Shock
Clinical syndrome representing an extreme state of circulatory failure
Impaired tissue perfusion leading to cellular dysfunction
Complex group of signs & symptoms that can be caused by a variety of factors
Clinical Manifestations of Shock
Directly related to pathophysiologic mechnaisms are involved. Progression is variable & depends on:
-Patient age & prior state of health Duration of shock state Response to treatment Correction of treatable cause
3 Stages of Shock
Early or compensatory
Intermediate or progressive
Late or irreversible
Classification Vascular Tone (Distributive)
Neurogenic Septic Anaphylactic
Intravascular Volume Hypovolemic
Ability of heart to act as pump Cardiogenic
Hemodynamic Changes
CO CVP SVR PAP PAWP
Distributive ↑or↑ ↓or↑ ↓or↑ ↓or↑ ↓or↑
Hypovolemic ↓ ↓ ↑ ↓ ↓
Cardiogenic ↓ ↑ ↑ ↑ ↑
Treating Shock States
Position: Supine/let elevation (if possible)
Trendelenberg should be avoided: Initiates aortic & carotid sinus reflex Impaired cerebral blood flow Decreased filling of coronary arteries
Fluids
Shock almost always involves a decrease in effective circulating volume
Need for volume expansion Fluid challenge
Septic Shock
Occurs in patients as a result of overwhelming infection
More common in infants, elderly & immuno-compromised
Clinical presentation can be subtle in elderly, debilitated or malnourished patients
Warm Shock
Vasodilation → ↓ SVR ↑ or normal CO
BP ↓ but skin is pink, warm & dry
Urine output is adequate
Cold Shock
Vasoconstriction ↓ ↑ SVR ↓ CO ↓ BP ↓ Urine output Metabolic Acidosis
Hypovolemic Shock
Loss of intravascular volume ↓
Decreased venous return to heart ↓ Circulatory insufficiency ↓ Inadequate tissue perfusion
Cardiogenic Shock
Pump failure Occurs when the heart can no
longer efficiently pump blood. CO is significantly decreased
Major cause: extensive myocardial injury secondary to MI
Treatment of Cardiogenic Shock
Treat reversible cause Goal of treatment is to:
Increase Cardiac Contractility Decrease Afterload (workload)
Careful fluid replacement (if needed) IABP insertion Drug therapy
Cardiac Performance
Low CO Cardiogenic Shock Dobutamine Vasodilator LABP Dopamine
Preload ↓ ↓ ↓ ↑Contractility ↑↑ - - ↑Afterload ↓ ↓↓ ↓ ↑Heart Rate - - - ↑MVO2 - ↓↓↓ ↓↓ ↑↑↑↑
Treatment of Peri-Op/Post-OpIschemia
Evaluate/Investigation of cause Drugs:
Belta Blockers Nitrates Vasopressors Calcium Blockers
Cardiac Arrhythmias
Atrial Fibrillation
Nearly 30% of patients undergoing coronary surgery & up to 50% of patients with valvular disease develop AF
Occurs in up to 5% of patients afterr any major surgery
Myocardial Ischemia
Myocardial Ischemia
Ischemia results from an imbalance between myocardial O2supply & demand.
Can be due to: ↑ Demand ↓ Supply Coronary Vasospasm
Causes of Ischemia Post-Op
Incomplete mycardial protection during aortic cross-clamp, incomplete revascularization, vasospasm, atheromatous emboli, thrombosis of native vessel or new graft
Myocardial revascularization patients are at higher risk of peri-op infarct than other CT surgery patients
Causes of Post-Op A-Fib
Common Causes Other Causes Electrolyte problems - Valve surgery Advanced age - History of RF Hypervolemia - Duration of x-
clamp CHF -CPB D/C of pre-op meds -Cardioplegia
method Hypoxia -Sepsis ETOH abuse
Treatment of AF
Prompt identification & treatment of cause
Chemical cardioversion First give drugs to treat rate Then drugs to convert to SR
Synchronized cardio version
Brady Arrhythmias Sinus Bradycardia Heart Blocks Cause:
Overuse of Beta blockers pre-op Manipulation or destruction of SA or
AV nodes Hypoxia Vagal stimulation
Treatment
Treat Cause
Pacing
Drugs
Ventricular Arrhythmias Range from occasional premature
beats to bigeminy, trigeminy, non-sustained VT to sustained VT & VF
Benign arrhythmias occur in 20-60% of patients post-op. Infrequently produce symptoms or require treatment
Incidence of sustained VT/VF after cardiac surgery = 0.4 -1.4%
Pre-disposing Factors in Development of VT
Myocardial ischemia Decreased CO Decreased EF (<40%) Metabolic derangements Drug interactions Hypoxemia
Cardiac Arrest
Ventricular Fibrillation
Uncoordinated continuous ventricular contraction which does not generate a cardiac output
Treatment: SHOCK! SHOCK! SHOCK!
Mortality increases 4-10% for every minute the first defibrillation attempt is delayed
Asystole
Complete absence of mechanical & electrical cardiac activity
Usually terminal event/Grim prognosis
Confirm rhythm! Check patient! If nay probability that rhythm is fine
VF shock should be attempted, otherwise not indicated
PEA Organized electrical activity without
effective cardiac contractions = no pulse!
Poor prognosis Identification & treatment of
reversible causes aides in restoring rhythm
Resuscitation is rare if reversible cause is not found
Open Cardiac Massage
Indications: Cardiac arrest associated with penetrating thoracic trauma, arrest during thoracic surgery or when chest wall deformity or recent sternotomy precludes effective closed massage
Pericarditis
Cause
Infections Uremia Neoplasm Radiation Rheumatic Fever Post-MI Post-Pericardiotomy
Clinical Manifestations
Occurs approximately 4 weeks post-op
Pain Friction rub Dyspnea Fever EKG changes Leukocytosis
Pericardial Effusion
Generally rapid accumulation of excess fluid within the pericardial space
May arise from acute pericarditis Large effusions may compress
adjoining structures & cause tamponade if left untreated
Tamponade
Compression of heart which decreases overall cardiac function dramatically
Clinical Signs Decreased CO patients who initially had
adequate ventricular performance Increased bleeding in early post-op
period with sudden decrease in drainage & hemodynamic worsening
May occur in patients with initial bleeding whose coagulation profile was corrected leading to formation of pericardial clot
Symptoms Rapid increase in R&L atrial pressure which
tends to equalize Muffled heart sounds Increased jugular venous pressure (distended
neck veins) Widening of mediastinum by CXR EKG changes Pulsus paradoxus (late effusion) Vague symptoms: LE edema, hepatomegaly,
pleural effusion (late)
Treatment
Surgery-re-exploration via median sternotomy
Sub-xiphoid incision Small right anterior thoracic
incision (late tamponade) Echocardiographic guided
puncture
Pneumothorax
Pneumothorax
Complete or partial collapse of a lung resulting from accumulation of air in the space between chest wall & lung (intrapleural space)
May be classified as either “open” or “closed”
Diagnosis
Clinical Presentation -Diagnostics: Dyspenea -Clinical
presentation & history
Pain -Chest x-ray Decreased air movement on affected side (decreased breath sounds)
Tension Pnuemothorax
Collection of air between chest wall & lung with no escape of air during expiration. This causes a rapid increase of air within pleural cavity, causing shifting of intrathoracic organs & increased intrathoracic pressure
Symptoms
Air hunger Violent agitation Cyanosis Tracheal deviation Subcutaneous emphysema
Treatment of Tension Pneumo
Rapid Assessment! CT insertion Insertion of large-b ore needle to
relieve intro-thoracic pressure Treatment of hypoxia
What happens in tension pneumothorax?
Infection
Mediastinitis
Infection of mediastinum resulting from inadequate healing after median sternotomy, potentially involving all structures of the mediastinum & chest wall
Treatment of Mediastinitis
Appropriate antibiotic coverage Complete sternal resection Use of closed irrigation/drainage
system Wound closure with muscle flap
Clinical Manifestations
Sternal dehiscene Purulent drainage Pain associated with chest motion Fever Leukocytosis + Wound cultures
Pathogenesis
All patients undergoing cardiac surgery especially when CPB is used are potential candidates for infection because of depressed inflammatory response & large exposure of blood elements to foreign materials which increases chances of contamination
Common Pathogens
Staph aureus Staph epidermis Gram negative bacteria Fungi Mixed flora
Risk Factors Diabetes COPD Bilateral mammary Smoking Prolonged ventilation Obesity Age >70 Use of bone wax Chronic renal failure Long operative time Excessive use of cautery
Prevention
Handwashing by staff Antiseptic pre-op soap showers by patient Careful trimming of skin hair just prior to
surgery Aggressive treatment of elevated glucose in
diabetic patients Maintenance of sterility during all invasive
procedures Use of minimal amount of bone wax Judicious use of cautery Prophylactic antibiotics
Avoid Bilateral IMA in patients with
Diabetes COPD Immunosupperssion Morbid obesity
Use of bone wax Indiscriminate use of cautery Cross contamination
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