Transcript File - Cardiac Education

COMPLICATIONS OF
CARDIOTHORACIC
SURGERY
Jacqueline Palmer-Powell, RN
Nurse Educator/CNS
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Complications Commonly
Resulting From CardioThoracic Surgery
CVA
CVA
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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
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Prior history of stroke, HTN, DM
Carotid disease, carotid bruit
Advanced age
Atrial Fib
Diagnosis & Treatment
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CT Scan demonstrates cerebral infarct
within 1-2 days
No treatment exist other than palliative
Early rehabilitation
Family counseling
Hypotension
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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
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Pre-op
Acute MI treated with
thrombolytics (failed)
Aspirin
IIBIIIA Platelet
Co-morbid states
(uremia, liver disease)
Post-op
- Vigorous chest
tube stripping
- Hypertension
- Heparin
What Constitutes Excessive
Bleeding?
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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
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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
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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
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Complete History
- Questions about previous surgery,
family history, bruising, heavy menses
- medication history (Prescribed, OTC &
herbal)
Physical Exam
Blood Work
Pre-op Bleeding Prevention
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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
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Aspirin
NSAIDS
IIBIIIA Platelet Inhibitors
Coumadin
Thrombolytics
Heparin
Prevention & Treatment of
Bleeding in OR
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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
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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
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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
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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
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<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
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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
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Treatment of LCOS
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Heart rate manipulation
Preload
Afterload
Myocardial Contractility
SHOCK
Shock
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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
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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
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Early or compensatory
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Intermediate or progressive
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Late or irreversible
Classification
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Vascular Tone (Distributive)
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Intravascular Volume
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Neurogenic
Septic
Anaphylactic
Hypovolemic
Ability of heart to act as pump
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Cardiogenic
Hemodynamic Changes
CO
CVP
SVR
PAP
PAWP
↑or↑ ↓or↑ ↓or↑
↓or↑
Hypovolemic
↓
↓
↑
↓
↓
Cardiogenic
↓
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↑
↑
↑
Distributive
↓or↑
Treating Shock States
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Position: Supine/let elevation (if
possible)
Trendelenberg should be avoided:
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Initiates aortic & carotid sinus reflex
Impaired cerebral blood flow
Decreased filling of coronary arteries
Fluids
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Shock almost always involves a
decrease in effective circulating volume
Need for volume expansion
Fluid challenge
Septic Shock
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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
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Vasodilation → ↓ SVR ↑ or normal CO
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BP ↓ but skin is pink, warm & dry
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Urine output is adequate
Cold Shock
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Vasoconstriction ↓ ↑ SVR
↓ CO
↓ BP
↓ Urine output
Metabolic Acidosis
Hypovolemic Shock
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Loss of intravascular volume
↓
Decreased venous return to heart
↓
Circulatory insufficiency
↓
Inadequate tissue perfusion
Cardiogenic Shock
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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
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Treat reversible cause
Goal of treatment is to:
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Increase Cardiac Contractility
Decrease Afterload (workload)
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Careful fluid replacement (if needed)
IABP insertion
Drug therapy
Cardiac Performance
Low CO
Dobutamine
Preload
Contractility
Afterload
Heart Rate
MVO2
↓
↑↑
↓
-
Cardiogenic Shock
Vasodilator
↓
↓↓
↓↓↓
LABP
Dopamine
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↓↓
↑
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↑↑↑↑
Treatment of Peri-Op/Post-Op
Ischemia
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Evaluate/Investigation of cause
Drugs:
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Belta Blockers
Nitrates
Vasopressors
Calcium Blockers
Cardiac Arrhythmias
Atrial Fibrillation
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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
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Ischemia results from an imbalance
between myocardial O2supply &
demand.
Can be due to:
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↑ Demand
↓ Supply
Coronary Vasospasm
Causes of Ischemia Post-Op
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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
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Common Causes
Other Causes
Electrolyte problems
Advanced age
Hypervolemia
CHF
D/C of pre-op meds
method
Hypoxia
ETOH abuse
- Valve surgery
- History of RF
- Duration of x-clamp
-CPB
-Cardioplegia
-Sepsis
Treatment of AF
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Prompt identification & treatment of
cause
Chemical cardioversion
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First give drugs to treat rate
Then drugs to convert to SR
Synchronized cardio version
Brady Arrhythmias
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Sinus Bradycardia
Heart Blocks
Cause:
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Overuse of Beta blockers pre-op
Manipulation or destruction of SA or AV
nodes
Hypoxia
Vagal stimulation
Treatment
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Treat Cause
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Pacing
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Drugs
Ventricular Arrhythmias
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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
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Myocardial ischemia
Decreased CO
Decreased EF (<40%)
Metabolic derangements
Drug interactions
Hypoxemia
Cardiac Arrest
Ventricular Fibrillation
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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
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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
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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
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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
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Infections
Uremia
Neoplasm
Radiation
Rheumatic Fever
Post-MI
Post-Pericardiotomy
Clinical Manifestations
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Occurs approximately 4 weeks post-op
Pain
Friction rub
Dyspnea
Fever
EKG changes
Leukocytosis
Pericardial Effusion
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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
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Clinical Signs
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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
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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
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Surgery-re-exploration via median
sternotomy
Sub-xiphoid incision
Small right anterior thoracic incision
(late tamponade)
Echocardiographic guided puncture
Pneumothorax
Pneumothorax
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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
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Clinical Presentation
-Diagnostics:
Dyspenea
-Clinical
presentation
&
history
 Pain
-Chest x-ray
 Decreased air movement
on affected side (decreased
breath sounds)
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Tension Pnuemothorax
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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
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Air hunger
Violent agitation
Cyanosis
Tracheal deviation
Subcutaneous emphysema
Treatment of Tension Pneumo
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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
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Infection of mediastinum resulting from
inadequate healing after median
sternotomy, potentially involving all
structures of the mediastinum & chest
wall
Treatment of Mediastinitis
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Appropriate antibiotic coverage
Complete sternal resection
Use of closed irrigation/drainage system
Wound closure with muscle flap
Clinical Manifestations
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Sternal dehiscene
Purulent drainage
Pain associated with chest motion
Fever
Leukocytosis
+ Wound cultures
Pathogenesis
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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
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Staph aureus
Staph epidermis
Gram negative bacteria
Fungi
Mixed flora
Risk Factors
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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
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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
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Bilateral IMA in patients with
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Diabetes
COPD
Immunosupperssion
Morbid obesity
Use of bone wax
Indiscriminate use of cautery
Cross contamination