Cardiac anesthesia board lecture

CARDIAC
ANESTHESIA
By:
Dr. Othman Ismat Abdulmajeed
Consultant Cardiac Anesthetist
Hawler Medical College
othman.abdulmajeed@med.hmu.edu.iq
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Dr.Othman Abdulmajeed

Pre-operative assessment
- Pre-operative tests ?
- Evaluation of LV function:
1- History.
2- Symptoms and clinical signs of left ventricular failure
3- Cardiac catheterization, CT angiography, and echocardiography
4- Ejection fraction (normally 65%)
5- LVEDP or PAOP: normal 6 to 15 mm Hg
6- Myocardial viability studies (contrast echocardiography or
positron emission tomography study)
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- Major determinants of myocardial oxygen consumption.. 
The three major determinants of myocardial oxygen consumption are :-

1-myocardial wall tension.

2-contractility. 3- HR.

- Factors determining myocardial oxygen supply

Myocardial oxygen (O2) supply = coronary blood ﬂow × arterial O2
content

The coronary blood ﬂow depends on the following:

1- Diastolic aortic pressure (DAP).

2- LVEDP.

3- Patency of coronary arteries.

4- Coronary vascular tone.

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Chronic Medications..
- Digoxin : In order to prevent digitalis intoxication after CPB,
digitalis preparations are usually discontinued one half-life (1.5 to 1.7
days for digoxin, 5 to 7 days for digitoxin) before surgery. Digitalis
intoxication is quite possible, especially after CPB when acid-base
and electrolytes are abnormal.
- Metoprolol : The β-blocker (metoprolol) should be continued not
only up until surgery but also throughout the perioperative period.
In patients with unstable angina, sudden withdrawal of β-blocker may
produce an exacerbation of symptoms and may precipitate acute MI.
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• Potential benefits of β-adrenergic blockade in heart failure
include decreased HR and normalization of β-receptor
function.
• Slower HRs improve diastolic function by increasing the
diastolic filling time and myocardial perfusion and by
decreasing the myocardial oxygen consumption.
• If the patient who is on metoprolol develops hypotension
intraoperatively, then we first should think about the more
common causes of intraoperative hypotension, such as
hypovolemia, deep anesthesia, and surgical manipulation,
which should be corrected first.
• There are no specific antagonists for metoprolol. In rare
instances, it is necessary to administer atropine for
bradycardia or epinephrine, isoproterenol, glucagon, calcium,
or digitalis to counteract the negative inotropic state
associated with β-blockade.
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Intra-operative monitoring
• ECG , Lead II and V5.

• Arterial line for IBP and ABG.

• PA and CVP catheters

• Temperature, Lower esophageal.

• Urine output.

• ET co2, Pulse oximetry.

• TEE.

• BIS
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Monitoring..
• PA catheter and CVP catheter will be discussed in details
later on in CARDIAC MONITORING lecture. and ECHO will be
discussed in THE ECHO lecture in more details.

• ECG monitoring: Multiple-lead ECG monitoring provides the
best clinically available method of detecting perioperative
ischemia, therefore, leads II and V5 are the optimal leads for
intraoperative myocardial ischemia.

• If only one lead can be displayed, V5 should be used because
lead V5 has the greatest sensitivity: 75% intraoperatively and
89% during exercise treadmill testing.
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Allen's test
• used to detect the presence of adequate collateral ulnar
arterial circulation,The Allen's test is:
• (Demo the procedure)
• Normal—if the ﬂush appears in less than 7 seconds (presence
of adequate collateral connections between the superﬁcial
[ulnar] and deep [radial] palmar arches)
• Borderline—7 to 15 seconds
• Abnormal—greater than 15 seconds
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Induction of Anesthesia
• Midazolam 1 to 2 mg is given as soon as the standard monitors are
applied and prior to the arterial line is inserted (under local anesthesia)
• A smooth induction is essential to prevent hypotension, hypertension,
and tachycardia. Different techniques may be used to achieve a
smooth induction.
• For patients with good left ventricular function, anesthesia is induced
with fentanyl, 2 to 5 µg per kg, and propofol, 1 to 2 mg per kg.
• For patients with poor left ventricular function, potent inhalation agents
such as isoflurane, sevoflurane, and desflurane should be used
cautiously during induction of anesthesia because of their dose-
dependent reduction in myocardial contractility and systemic arterial
resistance.
• Alternatively, etomidate 0.2 mg per kg may be administered for
induction.
• However, it is more important to maintain stable hemodynamics than
the choice of induction anesthetic agents.
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Maintenance of Anesthesia
•Again, smooth anesthesia is essential to achieve a balance
between myocardial oxygen demand and supply. Different
agents and techniques may be used to accomplish the same
goal.
•A combination of fentanyl (or another synthetic opioid) and
isoflurane, sevoflurane, or desflurane (or propofol) is a popular
choice.
•The depth of anesthesia must be titrated to meet the
requirements of the varying intensities of surgical stimulation.
Skin incision and sternal splitting are very painful. However, the
strongest stimulation is usually from sternal retraction with the
self-retaining retractor.
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Inhalational Vs Intravenous ?
•Both inhalation, IV, and combined agents have been used
successfully.
•Both have advantages and disadvantages. Understanding the
cardiovascular effects of each anesthetic agent and careful
titration of each drug will improve the balance between
myocardial oxygen demand and supply.
•Early detection and appropriate control of the major
determinants of myocardial oxygen consumption (BP, HR,
PAOP) are mandatory if myocardial ischemia is to be avoided.
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Understanding the CVS effects of ..
• Isoflurane, desflurane, and sevoflurane all produce a dose-related
depression in ventricular function and vascular tonus.
• Out of all the volatile anesthetics, isoflurane causes the most reduction in
vascular tone and coronary vasodilation, suggesting the possibility of steal
syndrome in patients with CAD.
• All of the potent drugs decrease arterial pressure in a dose-related manner.
The mechanism of BP decrease includes vasodilation, myocardial
depression and decreased cardiac output, and decreased sympathetic
nervous system tone.
• Narcotics such as morphine and fentanyl at their clinical dose have minimal
cardiovascular effects. Both may cause bradycardia. Neither sensitizes the
heart to catecholamines or depresses myocardial function.
• High doses of morphine, 1 mg per kg, produce a significant decrease in
arterial BP and systemic vascular resistance accompanied by an average
750% increase in plasma histamine. On the other hand, high doses of
fentanyl, 50 µg per kg, do not produce any significant changes in BP,
vascular resistance, and plasma histamine levels.
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ST-segment depression,Rx..
• An ST-segment depression is indicating ischemia and should
be treated by:
• Increasing oxygen supply: correct hypotension (with IV
phenylephrine), hypoxemia, anemia. 
Decrease oxygen demand: correct hypertension, tachycardia,
and increased PAOP or CVP by deepening anesthesia with a
volatile agent or by using vasodilators (nicardipine or
nitroglycerin) or β-blockers (metoprolol, esmolol, or labetalol).
• All the major determinants of decreased oxygen demand have
to be considered and corrected to their normal levels.
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Prophylactic nitroglycerin..
• It has been reported that prophylactic administration of
nitroglycerin, 0.5 or 1.0 μg/kg/min, during fentanyl anesthesia in
patients undergoing CABG did not prevent myocardial ischemia
or reduce the incidence of perioperative MI.
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Rx. of Hypertension..
Hypertension is usually due to inadequate depth of anesthesia and/
or activation of the sympathoadrenal pathways that occurs with
stress/surgery. Rarely, it is due to fluid overloading. The treatment of
hypertension includes the following:
• Deepening the anesthetic level. Inhalation agents such as
isoflurane and sevoflurane are more effective than narcotics
because of their vasodilator effect.
• Administering vasodilators, when inhalation agents are not used
• Nicardipine. Dose: 0.5 µg/kg/min, titrate to effect
• Labetalol. Dose: 5-mg increments, titrate to effect
• Nitroglycerin produces more venodilation than arteriolar dilation.
Dose: 20 to 200 µg per minute IV drip titration or bolus in 20-µg
increments. It is important to note that this agent affects BP mainly
via venodilation, which frequently will drop preload and may lower
the cardiac output such that greater fluid intake may be required.
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Rx. of Hypotension..
Hypotension is usually caused by acute hypovolemia, deep
anesthesia, bradycardia, or ventricular failure. The treatment
options are as follows:
• Increase fluid infusion when CVP or PAOP is low.
• Lighten the level of anesthesia or use a vasoconstrictor:
phenylephrine, 0.1 mg IV increments, to correct vasodilation
produced by anesthesia.
• For bradycardia, epicardial pacing may be used to increase
the HR.
• Treat cardiac failure when PAOP is high and TEE shows
global hypokinesia: 1) Avoid deep level of anesthesia.
2) Restrict fluids. 3) Use Inotropes.
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B-blocker during surgery..
• Indications :-
1. ST-segment depression associated with tachycardia; no response to
deepening the level of anesthesia
2. Supraventricular tachycardia
3. Recurrent ventricular arrhythmias
• Contraindications :-
Asthma, reactive chronic obstructive pulmonary disease

Esmolol is cardioselective and appears to have little eﬀect on bronchial
or vascular tone at doses that decrease HR in humans. Esmolol is a
short-acting β-blocker with an elimination half-life of 9 minutes and a
pharmacologic half- life of 10 to 20 minutes. It has been used
successfully in low doses in patients with asthma. Esmolol is metabolized
rapidly in the blood by an esterase located in the erythrocyte cytoplasm.
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Blood Conservation..
• Autologous Transfusion.

• Preoperative use of Erythropoietin.

• Intra-operative Normovolemic Hemodilution.

• Intra-operative plasmapheresis.

• Pharmacologic Rx, ( Tranexamic acid ).

• Peri-operative blood salvage.
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Anti-coagulation
• Heparin has been used conventionally in doses of 300 (200 to
400) units per kg of body weight.
• After 2 hours of the initial dose, subsequent doses of 100 units
per kg are given for each additional hour of bypass. Because
there is marked individual variation, heparin doses are best
monitored by the ACT test.
• The normal control value of ACT is 105 to 167 seconds.
• A baseline value is determined before the administration of
heparin, and the test is repeated 3 to 5 minutes after heparin
is given and at intervals of 30 to 60 minutes thereafter.
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Laboratory Monitoring during
CPB..
Should be done at least once hourly.
1. Arterial blood gases are kept at normal range.
2. Venous PO2 should be 40 to 45 mm Hg.
3. Hematocrit maintained between 20% and 30%
4. Electrolytes Na+, K+, ionized Ca2+
5. ACT measured each hour and maintained above 400 to 480
seconds.
6. Blood sugar probably should be kept below 250 mg per dL.
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Hypothermia during CPB
• Hypothermia decreases oxygen consumption and helps to
preserve the function of tissues during a hypoxic or ischemic
insult.
• However, the balance between oxygen supply and demand
can be impaired by reductions in tissue oxygen delivery due to
increased blood viscosity, reduced microcirculatory flow, and a
leftward shift of the oxygen-hemoglobin dissociation curve.
21

Anesthesia during CPB
• Anesthesia is maintained with intermittent administration of IV
propofol, benzodiazepines, narcotic, and/or inhalation agents
through the pump oxygenator to achieve unconsciousness
and analgesia, to control BP, and to prevent shivering.
• Hypothermia itself produces anesthesia and prolongs the
action duration of IV agents by decreasing hepatic metabolism
and urinary excretion.
• Muscle relaxants are given to prevent diaphragmatic
movement that interferes with surgery and to prevent shivering
during hypothermia.
• Shivering may increase oxygen consumption to as high as
486% of normal.
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Myocardial Protection
• The most popular and effective method of protecting the
myocardium is to reduce myocardial oxygen demand by
hypothermia and cardioplegia.
• Hypothermia is induced by a combination of systemic blood
cooling by heat exchangers in the oxygenator.
• Cardioplegia reduces myocardial oxygen consumption and
provides optimal conditions for surgery, It contains:-
Potassium and magnesium to relax the heart, Bicarbonate to
raise the PH level to 7.4-7.8 to increase intracellular shift of K+
and to prevent metabolic acidosis from ischemia. also contains
glucose and insulin. GTN is added to dilate the coronaries.
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Pink Urine during CPB
• Pink urine is a sign of massive hemolysis. Hemolysis is mainly
associated with the frothing, violent turbulence, acceleration,
and shear forces of negative pressures generated by the
suction apparatus and is associated to a lesser degree with
the action of the pumps or with the gas-blood interface effects
in the oxygenator.
• The renal threshold for hemoglobin is 100 to 150 mg per 100
mL. It is advisable to maintain a high output of alkaline urine to
prevent possible tubular damage from acid hematin crystals,
which are converted from hemoglobin.
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Ca++ at end of CPB
• With hemodilution, the ionized calcium frequently falls to
approximately 1.5 to 1.8 mEq per L (normal 2.2 to 2.6 mEq per
L, 1.1 to 1.3 mmol per L). Calcium chloride, 0.5 to 1.0 g,
frequently is given to increase myocardial contractility and
reverse potassium cardioplegia.
• Calcium increases the inotropic state of the myocardium and
induces an increase in systemic vascular resistance that
outlasts the inotropic effects.
• β-Blockers, increase intracellular calcium but also promote its
reuptake into the sarcoplasmic reticulum and may be more
appropriate in this setting.
• Calcium salts should probably not be given to patients with
good ventricular function in the absence of hypocalcemia or
hyperkalemia.
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Blood Sugar during CPB
• Blood sugar levels are elevated during the perioperative
period with CPB, Hyperglycemia is most profound during
hypothermic CPB, with approximately 100% of patients
(diabetic and non-diabetic) achieving plasma glucose levels
greater than 200 mg per dL.
There are several reasons for this:
1. Starvation overnight.
2. Sympathoadrenal activation, in response to surgical stress.
3. Active cooling the body during bypass causes a profound
reduction in insulin production, induces peripheral insulin
resistance, and is associated with renal tubular impairment in
glucose regulation.
4. Dextrose containing cardioplegia.
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CPB effects on Coagulation
• Platelet dysfunction and thrombocytopenia are found on and
after CPB. Platelet dysfunction is the most common cause of a
bleeding problem following CPB after heparin is reversed and
surgical bleeding is controlled.
• Generally, platelet function returns to near- normal status 2 to
4 hours following CPB.
28

Post CPB Inotropic support..
The need for inotropic support after CPB is usually assessed by
the following
• Preoperative ventricular function (ejection fraction).
• Effectiveness of intraoperative myocardial protection.
• Adequacy of surgical repair.
• Duration of aortic cross-clamping and CPB.
• Patient's age.
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Post CPB, Protamine..
•Protamine, 1 mg is given to reverse each 100 units or 1 mg of
heparin initially administered. Only the initial dose of heparin is
counted. The subsequently added dose of heparin, to keep the
ACT level above 480 seconds, is not considered because of its
metabolism and elimination.
•The ACT test is repeated 10 minutes after the administration of
protamine.
•Heparin is a strong organic acid (polyanion). Protamine is a
strong organic base (polycation). They combine ionically to form
a stable salt and lose their own anticoagulant activity. Protamine
contains two active sites, one that neutralizes heparin and
another that exerts a mild anticoagulant effect independent of
heparin.
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Post-0p. complications
Cardiovascular:
• CHF, arrhythmias, low output syndrome, myocardial ischemia or infarction due
to surgical manipulation, prolonged CPB and aortic cross-clamp (coronary
ischemia), use of cardioplegic solution, and occlusion or kinking of grafts
Pulmonary:
Acute lung injury or adult respiratory distress syndrome due to the following:
• Decreased blood flow to the lung during total CPB
• Collapsed alveoli during CPB, resulting in decreased surfactant and decreased
distensibility
• Fluid overloading
• Hyperoxia during CPB
• Left ventricular failure
• Microemboli
• Reperfusion injury
• Inflammatory response
• Infections
• Transfusion-related lung dysfunction
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Complications. cont..
Renal
• Polyuria from hemodilution and diuretics.
• Oliguria from hypoperfusion
• Acute kidney injury :-
A. Hypoperfusion
B. Ischemia
C. Inflammatory response
D. Nephrotoxins (preoperative contrast dyes, antibiotics)
• Acute tubular necrosis
• Acute or chronic renal insufficiency.
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Complications. cont..
Hemorrhage
• Too much or too little protamine to reverse heparin
• Thrombocytopenia and decreased coagulation factors
• Qualitative and quantitative platelet defect.
• Disseminated intravascular coagulopathy
• Fibrinolysis with low levels of fibrinogen
• Poor surgical hemostasis
Embolism: due to air, destroyed or aggregated formed blood
elements, fat, endogenous and exogenous debris
Neurologic: stroke and neurocognitive dysfunction
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Weaning..
• Ventilator management, weaning strategy, and extubation time
vary significantly among centers practicing cardiac surgery.
• Historically, patients were weaned from the respirator the
following morning after surgery.
• Recently, if the operative course is smooth and if the patient is
hemodynamically stable, weaning and extubation can be
performed early (usually 2 to 6 hours after surgery).
• Early tracheal extubation (fast-track) after CABG surgery may
have cost benefits and improvement in resource use when
compared with late tracheal extubation.
34

Thank you
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Cardiac anesthesia board lecture

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