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