16.1 Anaesthesia for Cardiac Surgery and Cardiopulmonary Bypass Management

16.1 Anaesthesia for Cardiac Surgery and Cardiopulmonary Bypass Management

Cardiac anaesthesia demands a rigorous understanding of cardiovascular dynamics, extracorporeal technology, and myocardial preservation. Managing patients undergoing cardiac surgery requires reconciling severe structural lesions with the non-physiological states imposed by cardiopulmonary bypass (CPB).

---

1. Preoperative Evaluation and Risk Stratification in Cardiac Surgery

Preoperative assessment in cardiac surgical candidates quantifies functional reserve, identifies end-organ dysfunction, and stratifies perioperative morbidity and mortality using validated multivariable algorithms.

Operative Risk Prediction Models

Two major clinical risk scoring algorithms dominate contemporary cardiac surgical practice:

1. EuroSCORE II (European System for Cardiac Operative Risk Evaluation): Calculates predicted in-hospital mortality following cardiac surgery using patient-related factors (age, sex, renal impairment staged by creatinine clearance, extracardiac arteriopathy, poor mobility, prior cardiac surgery, chronic pulmonary disease, active endocarditis, critical preoperative state), cardiac factors (NYHA functional class, Canadian Cardiovascular Society [CCS] class 4 angina, left ventricular ejection fraction, recent myocardial infarction <90 days, pulmonary artery systolic pressure), and procedure-related factors (surgical urgency, elective vs urgent vs emergency vs salvage, weight of intervention [isolated CABG vs single non-CABG vs two procedures vs three or more procedures], and surgery on the thoracic aorta).
2. STS (Society of Thoracic Surgeons) Risk Model: Widely utilized internationally, calculating predicted 30-day mortality alongside specific morbidities: permanent stroke, prolonged mechanical ventilation (>24 hours), acute kidney injury requiring renal replacement therapy, deep sternal wound infection, and reoperation.

Coronary Angiogram Interpretation

Anaesthesiologists must systematically review coronary angiograms prior to surgery to anticipate regional ischemia and plan hemodynamic support:

• Coronary Dominance: Determined by which coronary artery gives rise to the posterior descending artery (PDA), which supplies the posterior third of the interventricular septum and the inferior wall of the left ventricle:
  • Right Dominant (~85%): PDA branches from the distal Right Coronary Artery (RCA).
  • Left Dominant (~10-15%): PDA branches from the Left Circumflex Artery (LCx).
  • Co-dominant (~5%): Posterior interventricular groove is supplied by branches from both the RCA and LCx.
• Significance Criteria: Luminal diameter reduction $\ge 70\%$ is considered hemodynamically significant in epicardial vessels (Left Anterior Descending [LAD], LCx, RCA). For the Left Main Coronary Artery (LMCA), luminal stenosis $\ge 50\%$ constitutes critical, life-threatening disease, predisposing to catastrophic global left ventricular ischemia during induction.
• Fractional Flow Reserve (FFR): Invasive physiological assessment of coronary stenosis during pharmacological hyperemia (intravenous adenosine). An FFR $\le 0.80$ confirms functionally significant myocardial ischemia warranting revascularization.

---

2. Valvular Heart Disease Pathophysiology and Hemodynamic Goals

Anaesthetic induction and maintenance must be tailored to the specific mechanical and loading constraints of each valvular defect.

Critical Clinical Distinctions:

• Aortic Stenosis: Concentric hypertrophy shifts the pressure-volume loop upward and to the left. The thick, non-compliant ventricle relies heavily on the atrial kick. Acute loss of sinus rhythm (e.g. junctional rhythm or atrial fibrillation) triggers immediate, profound hypotension. Tachycardia dramatically curtails diastolic coronary perfusion time while escalating oxygen demand, inducing subendocardial ischemia. Vasodilators (such as nitroprusside or high-dose ACE inhibitors) are hazardous because fixed outflow obstruction prevents compensatory increases in stroke volume, causing catastrophic systemic and coronary hypoperfusion. Phenylephrine is the vasopressor of choice for maintaining perfusion pressure without inducing tachycardia.
• Aortic Regurgitation: The regurgitant volume per beat is proportional to the duration of diastole ($t_{\text{diastole}}$) and the transvalvular diastolic pressure gradient ($DBP - LVEDP$). Bradycardia prolongs diastole, causing massive ventricular over-distension, acute pulmonary venous congestion, and subendocardial ischemia from elevated wall tension. The management rule of thumb is "fast, forward, and full".

---

3. Cardiopulmonary Bypass (CPB) Circuit Architecture

The CPB circuit mechanically substitutes for the functions of the heart and lungs, creating an extracorporeal loop that diverts venous blood, exchanges respiratory gases, modulates systemic temperature, and returns oxygenated blood to the arterial tree under controlled pressure.

  [ Systemic Veins (SVC / IVC) ]
                |
      (Venous Cannulae)
                v
     [ Venous Reservoir ]  <--- (Cardiotomy Suction & Vent Blood)
                |
                v
    [ Arterial Blood Pump ] ---> (Roller or Centrifugal)
                |
                v
    [ Membrane Oxygenator ] <---> [ Heat Exchanger (Water Bath) ]
                |
                v
    [ Arterial Line Filter ] (20-40 micron screen + Bubble Trap)
                |
      (Arterial Cannula)
                v
     [ Ascending Aorta ]

Circuit Components and Engineering Specifications

1. Venous Cannulation and Drainage:
   • Two-Stage Single Atriocaval Cannula: Inserted via the right atrial appendage into the inferior vena cava (IVC); drains IVC through the distal basket and superior vena cava (SVC) / right atrium via proximal side-holes. Standard for isolated CABG and aortic valve procedures where the right heart is not opened.
   • Bicaval Cannulation: Separate cannulae placed directly into the SVC and IVC, secured with tourniquets (caval snares / Rumel tourniquets). Mandatory for procedures opening the right heart (tricuspid/mitral valve surgery, ASD/VSD repair) to isolate the right heart chambers completely from venous return.
   • Drainage Mechanics: Primarily relies on siphon gravity drainage (reservoir positioned 40-70 cm below the patient's right atrium) or Vacuum-Assisted Venous Drainage (VAVD; applying negative pressure of $-20\text{ to }-40\text{ mmHg}$ to a sealed reservoir to facilitate drainage through smaller cannulae in minimally invasive surgery).
2. Venous Reservoir: Collects systemic venous return, acts as a compliant volume buffer, and houses a coarse mesh defoamer/filter to eliminate gross air bubbles before pumping.
3. Arterial Blood Pumps:
   • Roller Pumps: Positive displacement pumps utilizing rotating rollers that compress medical-grade silicone tubing against a semicircular raceway. Output is strictly dependent on roller RPM and tubing diameter, independent of afterload or preload. Hazards: True occlusion can generate extreme pressures ($>1000\text{ mmHg}$) if downstream obstruction occurs, risking line rupture or spallation of microparticles from tube wear. Inadvertent pumping of gross air if the reservoir runs dry.
   • Centrifugal Pumps: Non-occlusive magnetically coupled impellers or nested cones rotating at high speed (2000-3500 RPM). Blood is propelled by kinetic energy and centrifugal force. Flow is non-obligate and directly sensitive to both preload and afterload (if downstream pressure spikes, flow decreases to zero without line rupture). Hazards: Backward flow (retrograde siphonage) into the pump if the pump stops rotating while the arterial line is un-clamped.
4. Membrane Oxygenators: Contemporary oxygenators utilize hollow-fiber microporous polypropylene or polymethylpentene membranes. Venous blood flows over the external surface of microscopic hollow fibers while sweep gas ($O_2 / \text{Air}$ mixture) flows through the fiber lumina. Gas transfer occurs via passive diffusion across microscopic pores:
   • Oxygenation ($P_a\text{O}_2$) is controlled by adjusting the fraction of delivered oxygen ($F_i\text{O}_2$) in the sweep gas.
   • Carbon dioxide elimination ($P_a\text{CO}_2$) is controlled by altering the sweep gas flow rate (increasing sweep flow flushes $CO_2$ from the gas boundary layer, enhancing clearance).
5. Heat Exchanger: Integrated into the oxygenator; utilizes countercurrent warm or cold water circulating through stainless steel or polyurethane tubes to control blood temperature.
6. Arterial Line Filter: Screen filter with a pore size of 20 to 40 $\mu\text{m}$ placed between the oxygenator and the patient. It incorporates a one-way continuous purge line to capture gaseous microemboli, fat globules, and aggregate cellular debris before blood reaches the ascending aorta.

---

4. Priming Solution and Hemodilution Mechanics

The extracorporeal circuit must be primed with liquid to eliminate all air before connecting to the vasculature. The priming volume typically ranges from 1100 to 1500 mL of balanced crystalloid solution (e.g. Plasma-Lyte, Ringer's acetate/lactate), frequently supplemented with:

• Mannitol (0.5 g/kg or 12.5-25 g): Acts as an osmotic diuretic, scavenges oxygen-derived free radicals, and supports renal tubular patency during low-pressure bypass.
• Heparin (5,000 - 10,000 IU): Prevents thrombotic activation on foreign circuit surfaces upon initial blood contact.
• Sodium Bicarbonate: Buffers prime solution acidosis.
• Albumin 20% or Synthetic Colloids: Increases prime oncotic pressure to limit tissue edema.

Acute Normovolemic Hemodilution on CPB

When the patient's blood mixes with the crystalloid prime, acute hemodilution occurs. The resulting hematocrit ($Hct_{\text{CPB}}$) can be estimated by: $Hct_{\text{CPB}} = \frac{Hct_{\text{patient}} \times EBV}{EBV + V_{\text{prime}}}$ where $EBV$ is the patient's estimated blood volume (~$70\text{ mL/kg}$ in males, ~$65\text{ mL/kg}$ in females) and $V_{\text{prime}}$ is the circuit prime volume.

• Target Hematocrit: Maintained between 22% and 25% (hemoglobin ~7.0-8.5 g/dL) during hypothermic CPB.
• Physiological Rationale: Moderate hemodilution offsets the marked increase in blood viscosity induced by hypothermia (blood viscosity increases by ~2% for every 1°C fall in temperature), preserving microcirculatory capillary perfusion and preventing rheological stasis. However, excessive hemodilution ($Hct < 20\%$) compromises systemic oxygen delivery ($\dot{D}\text{O}_2$), impairs renal medullary oxygenation, and correlates with increased rates of perioperative acute kidney injury and stroke.

---

5. Anticoagulation for CPB, Heparin Resistance, and Protamine Reversal

Blood contact with the massive foreign surface area of the CPB circuit triggers immediate, catastrophic activation of the intrinsic coagulation pathway, contact system (Factor XII/kallikrein), and platelets. Flawless anticoagulation is mandatory.

Unfractionated Heparin (UFH) Protocol

• Dose: 300 to 400 IU/kg administered via central venous catheter or directly into the right atrium by the surgeon.
• Mechanism: Binds reversibly to antithrombin III (ATIII) via a specific high-affinity pentasaccharide sequence. This produces an allosteric conformational change that accelerates ATIII-mediated inactivation of thrombin (Factor IIa), Factor Xa, and Factors IXa, XIa, and XIIa by over 1,000-fold.
• Monitoring with Activated Clotting Time (ACT):
  • Baseline ACT is measured prior to heparin administration (normal baseline: 90-130 seconds).
  • Measurements utilize Kaolin (clay activator) or Celite (diatomaceous earth activator) cartridges.
  • Target ACT for CPB: Must exceed 400 to 480 seconds prior to cannulation of the aorta and throughout the bypass run.
  • ACT must be checked every 30 to 45 minutes on bypass; supplemental heparin (3,000-5,000 IU) is administered if ACT falls below 480 seconds.

Heparin Resistance

Defined as the inability to achieve an ACT $\ge 400\text{--}480\text{ seconds}$ despite the administration of a full weight-based heparin dose ($>400-500\text{ IU/kg}$).

• Primary Etiology: Congenital or acquired Antithrombin III Deficiency. Acquired ATIII deficiency is exceedingly common in patients receiving preoperative unfractionated or low-molecular-weight heparin (which depletes ATIII stores), patients with acute coronary syndrome, active infective endocarditis, sepsis, or liver cirrhosis.
• Management:
  1. Administer a second supplemental dose of heparin (5,000-10,000 IU).
  2. If ACT remains sub-therapeutic, administer Antithrombin III Concentrate (recombinant or human plasma-derived, 1,000-2,000 IU IV) or Fresh Frozen Plasma (FFP) (2 to 4 units; each unit contains ~1 IU/mL of functional ATIII).

Protamine Reversal and Adverse Reactions

Upon complete cessation of CPB and stable decannulation, heparin is reversed with Protamine Sulfate, a strongly basic, low-molecular-weight polycationic protein derived from salmon sperm. Protamine binds ionically to strongly acidic, polyanionic heparin, creating a stable, inactive neutral salt precipitate that eliminates anticoagulant activity.

• Dosing: 1 mg of protamine neutralizes approximately 100 IU of active circulating heparin (titrated based on time elapsed since heparinization, typically 0.6-0.8 mg per 100 IU initial dose if >1-2 hours have elapsed).

                      [ PROTAMINE ADVERSE REACTIONS ]
                                     |
     +-------------------------------+-------------------------------+
     |                               |                               |
[ Type I: Rapid Injection ]      [ Type II: Anaphylaxis ]     [ Type III: Pulmonary HTN ]
 - Non-immunological histamine    - IgE-mediated anaphylaxis   - Complement-mediated C5a
   & bradykinin release             or anaphylactoid             thromboxane A2 release
 - Peripheral vasodilation        - Bronchospasm, flushing,    - Severe pulmonary vasoconstriction
 - Transient hypotension            angioedema, shock          - RV failure & acute low output
 - Prevention: Slow IV over       - Risk: NPH insulin, fish    - Treatment: Stop protamine, inotropes,
   10-15 minutes                    allergy, post-vasectomy      pulmonary vasodilators, resume CPB

---

6. Myocardial Protection and Cardioplegia Delivery

Surgical repair of intracardiac structures necessitates a quiet, bloodless, flaccid heart, achieved by cross-clamping the ascending aorta. Without protection, normothermic myocardial ischemia causes irreversible necrosis within 15 to 20 minutes.

Biophysical Principles of Cardioplegic Arrest

• Mechanisms of Metabolic Arrest: Infusion of a hyperkalemic cardioplegic solution into the coronary circulation rapidly elevates extracellular potassium ($[K^+]_e = 16\text{--}20\text{ mmol/L}$). According to the Nernst equation: $E_K = \frac{RT}{F} \ln \left( \frac{[K^+]_e}{[K^+]_i} \right)$ Elevated extracellular potassium depolarizes the resting membrane potential of cardiomyocytes from $-90\text{ mV}$ toward approximately $-50\text{ mV}$. At this partially depolarized voltage, fast voltage-gated sodium channels are permanently inactivated, blocking Phase 0 depolarization and arresting electrical conduction and mechanical contraction in diastole.
• Metabolic Sparing: Halting mechanical electromechanical work cuts myocardial oxygen consumption ($M\dot{V}\text{O}_2$) by ~90%. Concomitant myocardial cooling to 4°C to 10°C reduces basal metabolic oxygen requirements by an additional factor of 2 for every 10°C drop ($Q_{10} \approx 2$), lowering ischemic $M\dot{V}\text{O}_2$ to $<5\%$ of baseline normothermic contracting levels.

Cardioplegia Formulations and Delivery Modalities

• Cold Crystalloid Cardioplegia (e.g. St. Thomas' Hospital Solution, Bretschneider/Custodiol, Del Nido): Crystalloid carrier containing balanced electrolytes, high potassium, magnesium (stabilizes membrane), procaine or lidocaine (sodium-channel blockade), and buffers. Del Nido cardioplegia incorporates lidocaine and mannitol, allowing single-dose administration providing 60 to 90 minutes of safe arrest.
• Cold Blood Cardioplegia (e.g. 4:1 or 8:1 Blood-to-Crystalloid): Delivers autologous blood mixed with hyperkalemic crystalloid. Advantages include physiological oxygen-carrying capacity (via hemoglobin), endogenous buffering capacity (via histidine residues on hemoglobin and plasma proteins), and physiological oncotic pressure.
• Warm Blood Cardioplegia ("Hot Shot"): A warm, substrate-enriched blood infusion (normokalemic, supplemented with aspartate/glutamate) administered immediately prior to aortic cross-clamp removal to replenish myocardial ATP and accelerate functional recovery upon reperfusion.
• Delivery Routes:
  • Antegrade Cardioplegia: Administered into the aortic root proximal to the cross-clamp or directly into coronary ostia via handheld cannulae. Relies on an intact aortic valve; ineffective in severe aortic regurgitation, where fluid flows directly into the LV, causing severe LV distension and zero coronary delivery.
  • Retrograde Cardioplegia: Cannula placed into the coronary sinus via the right atrium; flows backwards through the cardiac venous system into coronary capillary beds. Essential in severe aortic regurgitation or high-grade multivessel coronary artery occlusions that prevent antegrade flow.

---

7. Systemic Hypothermia and Circulatory Arrest

Therapeutic hypothermia reduces global cerebral and systemic metabolic rate, extending the safe window of ischemic tissue viability.

Temperature Categories and Circulatory Arrest

• Mild Hypothermia: 32°C to 35°C (standard for routine CABG and valve surgery).
• Moderate Hypothermia: 28°C to 32°C (used for complex resections or mitral repairs).
• Deep Hypothermic Circulatory Arrest (DHCA): Core temperature cooled to $<20\text{--}24\text{°C}$ (typically 18°C). Used for complex aortic arch reconstruction (e.g. type A aortic dissection, elephant trunk procedure) where placement of an aortic cross-clamp is anatomically impossible. At 18°C, the cerebral metabolic rate ($CMRO_2$) is reduced to ~18-20% of baseline, permitting safe total circulatory arrest for 30 to 40 minutes without gross neurological deficit.
• Adjunctive Neuroprotection during DHCA:
  • Topical craniocervical hypothermia (ice packed around head).
  • Pharmacological metabolic suppression (propofol, thiopental) to achieve electroencephalographic (EEG) burst suppression.
  • Selective Antegrade Cerebral Perfusion (SACP): Cannulation of the right axillary / subclavian artery or brachiocephalic artery, perfusing the brain with cold blood (10-15 mL/kg/min; line pressure 40-70 mmHg) during distal arch reconstruction.
  • Retrograde Cerebral Perfusion (RCP): Infusion of cold oxygenated blood retrogradely through the superior vena cava cannula (pressure maintained $<25\text{ mmHg}$ to prevent cerebral edema).

Temperature-Corrected Acid-Base Management on CPB

---

8. Systematic Weaning from Cardiopulmonary Bypass

Separation from CPB transfers the circulatory workload back from the extracorporeal machine to the patient's heart and lungs. It must follow a structured, multi-system checklist.

The "WARM & STEADY" Weaning Protocol

1. W - Warm: Patient re-warmed to target core (bladder/rectal) temperature $\ge 36.5\text{°C}$ and nasopharyngeal temperature $\le 37.5\text{°C}$ (avoid hyperthermic cerebral injury). Peripheral temperature $>35\text{°C}$ to ensure absence of severe peripheral vasoconstriction.
2. A - Air Cleared: Thorough de-airing of left-sided cardiac chambers (LA, LV, aortic root vent) verified by transesophageal echocardiography (TEE) under surgical agitation, Valsalva ventilation maneuvers, and steep Trendelenburg positioning.
3. R - Rhythm: Normal sinus rhythm, rate 80 to 100 bpm. Ventricular pacing, AV sequential epicardial pacing, or pharmacological cardioversion/defibrillation initiated if bradycardia, heart block, or tachyarrhythmias persist.
4. M - Metabolic & Electrolytes: Arterial blood gas confirmation: $K^+ 4.0-5.0\text{ mmol/L}$, ionized calcium ($iCa^{2+}$) $>1.0-1.1\text{ mmol/L}$, hematocrit $>22-25\%$, $pH 7.35-7.45$, base deficit $< -3\text{ mmol/L}$, lactate clearing.
5. S - Stable Ventilation: Mechanical ventilation re-instituted with 100% $O_2$, tidal volumes 6-8 mL/kg, PEEP 5 cmH$_2$O. Lungs visually inspected for symmetrical bilateral inflation and expansion.
6. T - Tone & Inotropic Support: Baseline inotropic/vasopressor infusions established (e.g. norepinephrine for vasoplegic low SVR, milrinone or epinephrine for biventricular systolic failure, vasopressin for refractory vasoplegia).
7. E - Echocardiography: TEE evaluation of biventricular loading and function: global and regional LV systolic performance, RV fractional area change (FAC), patent coronary graft flows, competence of reconstructed valves, absence of dynamic LVOT obstruction.
8. A - Access & Calibration: Arterial line zeroed at the phlebostatic axis (or circle of Willis); CVP and pulmonary artery catheters transduced and calibrated.
9. D - Drainage Clamped: Perfusionist slowly clamps the venous drainage line, allowing ventricular chambers to fill with blood from the reservoir. Pump output is progressively reduced from full flow (100%) to partial flow (75%, 50%, 25%) while systemic blood pressure and filling pressures (CVP, PCWP, or direct LA line) are observed.
10. Y - You are Off! Flow terminated. Once hemodynamic stability is documented over several minutes, the venous cannula is removed, followed by the arterial cannula, and slow protamine administration begins.

---

9. Intra-Aortic Balloon Pump (IABP) Counterpulsation

The IABP is a temporary mechanical circulatory support device positioned percutaneously via the femoral artery into the descending thoracic aorta. Its tip sits 1 to 2 cm distal to the origin of the left subclavian artery, positioned above the renal artery branches.

                 [ Aortic Pressure Waveform with IABP 1:2 ]

   Pressure
     ^                  Augmented Diastolic
     |                       Peak (PDP)
     |                        / \
     |    Normal             /   \             Assisted
     |    Systole           /     \            Systole
     |     / \             /       \             / \
     |    /   \  Dicrotic /         \           /   \
     |   /     \  Notch  /           \         /     \
     |  /       \  __   /             \       /       \
     | /         \/  \ /               \     /         \
     |/               v                 \___/           \___
     +--------------------------------------------------------> Time
                      ^                     ^
                  Inflation             Deflation
              (at Dicrotic Notch)   (before Systole)

Physiological Principles of Counterpulsation

1. Diastolic Inflation (Augmentation):
   • Timing: Rapid inflation with helium gas occurs precisely at the dicrotic notch of the aortic pressure waveform (marking aortic valve closure and the onset of diastole).
   • Hemodynamic Consequence: Displaces blood retrograde toward the aortic root, significantly increasing diastolic aortic root pressure (Peak Diastolic Pressure [PDP]). Because coronary blood flow occurs almost exclusively during diastole, this dramatically enhances Coronary Perfusion Pressure ($CPP = DBP - LVEDP$) and oxygen delivery to the myocardium.
2. Presystolic Deflation (Afterload Reduction):
   • Timing: Deflates rapidly immediately before ventricular systole (during the isovolumetric contraction phase, just prior to opening of the aortic valve).
   • Hemodynamic Consequence: The sudden evacuation of balloon volume creates a localized vacuum, dropping aortic end-diastolic pressure (Reduced Aortic End-Diastolic Pressure [BAEDP]). The left ventricle ejects against substantially lower vascular impedance, reducing LV peak systolic pressure, ventricular wall stress, and myocardial oxygen demand ($M\dot{V}\text{O}_2$), while augmenting stroke volume and cardiac output by 15% to 20%.

Synchronization, Triggers, and Contraindications

• Triggers: Electrocardiographic R-wave (most common; balloon deflates on R-wave detection and inflates at the middle of the T-wave) or arterial pressure waveform tracking (inflates at the dicrotic notch and deflates at the end-diastolic upstroke).
• Absolute Contraindications:
  • Moderate-to-Severe Aortic Regurgitation: Diastolic balloon inflation forcefully directs blood retrogradely through the incompetent aortic valve into the LV, producing catastrophic acute LV distension, pulmonary edema, and zero augmentation.
  • Aortic Dissection: Risk of balloon placement into the false lumen or propagating the intimal flap.
  • Severe Thoracic Aortic Aneurysm: Risk of rupture.
• Relative Contraindications: Severe peripheral vascular disease (iliofemoral atherosclerosis, risk of limb ischemia), descending thoracic aortic stents, uncontrolled coagulopathy.