Determinants of myocardial oxygen supply and demand
Coronary blood flow to the left ventricle occurs only during diastole. Increased heart rate decreases the diastolic interval, with little change in the length of systole.
Myocardial oxygen supply depends upon:
- O2 content of arterial blood (Hb and SaO2).
- Myocardial (coronary) blood flow; this is further determined by Coronary flow = (ADP - LVEDP) / resistance
- Diastolic blood pressure (dependent upon systolic pressure and heart rate).
- Diastolic interval (length of diastole, again dependent upon heart rate).
- Blood viscosity (decreased on cardiopulmonary bypass).
- Coronary vascular resistance (variable coronary vascular tone and fixed atheromatous lesions).
- LVEDP (higher pressures decrease flow).
Myocardial oxygen demand depends upon:
• Myocardial wall tension (systolic blood pressure).
• Number of contractions per minute (i.e. heart rate).
• ‘Physiological’ heart rates and systemic arterial pressures provide optimal coronary flow.
- Bradycardia provides long diastolic intervals and hence more time for coronary blood flow, together with few contractions demanding oxygen, but falling diastolic pressure during prolonged diastole decreases coronary perfusion pressure and hence CBF becomes limited in late diastole.
- Tachycardia increases mean diastolic pressure and hence coronary perfusion pressure but allows relatively little time for the flow to occur; increased numbers of contractions also increase myocardial O2 consumption.
- High blood pressure provides higher diastolic pressures for improved coronary perfusion and hence O2 supply, but generation of increased systolic pressures increases O2 consumption.
- Low blood pressures are generated by low myocardial wall tension, and hence low systolic pressures and O2 demand, but the associated low diastolic pressure limits coronary blood flow and hence O2 supply.
Phases of a CABG case
- *Cardiac theatre setup**
- Invasive monitoring devices - arterial line, CVC/PAC, TOE, temp probe
- BIS
- Medication availability - vasopressors, inotropes, vasodilators, heparin, anti-arrhythmics
- Defibrillator and pacing box
- Fluid warmer
- *Pre-induction:**
- Anxiolysis
- Cross-match
- Establish invasive and standard monitoring
- ICU bed availability
- *Pre-bypass:**
- TOE
- Conduit harvest
- Sternotomy
- Heparinisation
- Cannulation for CPB
- *CPB:**
- Pre-clamp
- Cross-clamp
- Post-clamp
- *Post-bypass:**
- Decannulation
- Closure
- Transfer to ICU
What is cardiopulmonary bypass? How does a heart-lung machine work?
CPB replaces the function of heart and lungs while the heart is arrested, allowing for a bloodless and stable surgical field.
- Membrane oxygenators are most commonly used. These contain minute hollow fibres, giving a large surface area for gas exchange (2–2.5m2). Gas exchange occurs down concentration gradients; increasing the gas flow removes more CO2 and increasing FiO2 increases oxygenation.
- Prior to CPB, full anticoagulation of the patient is required, with an activated clotting time (ACT) recorded at >400s.
- The bypass circuit is primed with crystalloid (e.g. Hartmann’s solution), heparin, and occasionally mannitol. The bypass machine normally delivers non-pulsatile flow of 2.4l/min/m2 (to correspond to a typical cardiac index).
- Mean arterial pressure (MAP) is normally maintained between 50 and 70mmHg by altering systemic vascular resistance (SVR).
- Volume, as crystalloid/colloid/blood, can be added to or removed by ultrafiltration, to maintain a haematocrit of 20–30%.
Complications of cardiopulmonary bypass
- CPB causes haemolysis, platelet damage, and consumption of coagulation factors. This is usually minimal for the first 2hr.
- Other problems include poor venous drainage, aortic dissection, and gas embolisation.
- Risk of a cerebrovascular episode (CVE) ranges from 1–5% and is associated with increasing age, hypertension, aortic atheroma, previous CVE, diabetes, and type of surgery (aortic arch replacement > valve replacement > coronary artery surgery).
Hypoperfusion and emboli are the main aetiological factors. Strategies to reduce cerebral injury (thiopental, steroids, mannitol, use of arterial filters in the bypass circuit) lack an evidence base. Maintaining optimum perfusion pressures, normoglycaemia, scrupulous surgical de-airing of the heart, and careful temperature control may decrease the incidence of neurological sequelae.
Induction and pre bypass phase of a cardiopulmonary bypass anaesthetic
Aim is to induce unconsciousness with maximal haemodynamic stability
- Confirm monitoring, drugs, perfusionist and surgeons are prepared (especially if critical aortic stenosis, left main disease, tamponade or ischaemia)
- Antibiotic
- Midazolam
- Fentanyl 10-15 mcg/kg
- Either inhalational induction with sevoflurane or IV propofol TCI 2mcg/ml
- Vasopressors as needed
- Vecuronium 10mg +/- pancuronium 4-8mg
- Tranexamic acid 1g followed by 500mg/hr infusion
- Ventilate and intubate
- Bite block and TOE probe
Cannulation of aorta
↓ SBP to 80-100mmHg to reduce risk aortic dissection
Commencing cardiopulmonary bypass (HADES)
- Heparin 300 units/kg (and pre-heparin ACT/ABG/TEG)
- ACT > 400s
- Drugs – anaesthetic, analgesia, NMB
- Emobli (no air in CPB cannulae)
- SGC - pull back PAC
- Turn off lungs but keep low O2 flows (1-2L/min) to prevent negative pressure from continued O2 uptake
- Vaporiser off and inform perfusionist if drug to be given via CPB machine
- Monitor BIS
- Monitor ABG and ACT at least q30min
Concluding cardiopulmonary bypass (WARM LIP)
Venous line is progressively clamped and heart allowed to fill/eject (usually relatively underfilled to prevent overdistension of poorly functioning ventricles).
- Warm > 36°C (nasopharyngeal)
- ABG: K 4.5 – 5.0 mmol/L; HCT > 20%; normal pH
- Rhythm (SR or paced at 88 AOO - atrial pacing, no sensing and no sensing response)
- Monitors on
- Lungs expanded and ventilating
- Infusions (inotropes) running and in the patient
- Perfusion - LV must be able to eject and K normal. Consider IABP if poor contractility on TOE
Anaesthesia post cardiopulmonary bypass
- Protamine 3mg/kg via peripheral IV (i.e. 1mg per 100 units heparin administered) after full wean from CPB: test dose 10-20mg then 20-30mg/min up to 1/3 total dose then surgeons will decannulate aorta. Give remainder of dose after aortic cannulation site secured. Target ACT 105-140s. May require platelets due to dysfunction induced by CPB.
- Decannulation requires SBP <100; maintain SBP 100-140mmHg otherwise
Closure of pericardium (may worsen myocardial compliance and necessitate fluids/vasopressors); closure of sternum reduces chest wall compliance
Pacing modes post bypass - asynchronous, single chamber demand and dual chamber modes
Chamber Paced
chamber sensed
response to sensing
V = Ventricle
V = Ventricle
I = Inhibited
A = Atrium
A = Atrium
T = Triggered
O = None
O = None
O = None
D = Dual
D = Dual
D = Dual (I & T)
Asynchronous: AOO, VOO, DOO – paces regardless of underlying electrical activity and competes with intrinsic rhythm. This is the usual response to placing a magnet over the pacemaker and is also useful when pacing and diathermy used simultaneously.
Single chamber demand – single chamber pacing inhibited by intrinsic activity: AAI (sinus node dysfunction with intact AV conduction), VVI (if heart block, AF or flutter)
Dual chamber: AV synchronous (VAT, VDD); AV sequential
AAI - for sinus bradycardia
AOO - for sinus bradycardia and ignores diathermy (MOST USEFUL POST CPB)
VVI - for bradycardia if heart block
DDD - AV sequential pacing
DOO - emergency mode
IF ASYNCHRONOUS PACING THEN APPLY EXTERNAL DEFIB PADS DUE TO R ON T PHENOMENON!!
What is cardioplegia and how is it administered? Cold vs warm cardioplegia.
Ringer’s solution containing potassium (20mmol/l), magnesium (16mmol/l), and procaine.
Can be blood or crystalloid based. The advantages of blood cardioplegia are largely theoretical and based on the assumption that haemoglobin will carry oxygen and thus help reduce myocardial damage.
When rapidly infused (1 litre) this renders the heart asystolic.
Cold (4°C) cardioplegia affords myocardial protection against ischaemia. Further doses (500ml) are repeated every 20min or when electrical activity returns.
Reperfusion (warm blood) cardioplegia is sometimes used towards the end of bypass to wash out products of metabolism.
Cardioplegia is usually administered anterograde (via the coronary arteries), but retrograde cardioplegia may be delivered via the coronary sinus (in which case, monitor infusion pressure).
Management of massive CPB air embolus
Stop pump, steep Trendelenberg, thiopentone, rapid cooling, de-air pump, retrograde perfusion
Pre-operative assessment for cardiac surgery: EuroSCORE and minimum investigations
Risk assessment using EuroSCORE (European System for Cardiac Operative Risk Evaluation) to calculate percentage mortality:
- Patient factors: age >60, female sex, COPD, peripheral / cerebral / coronary vascular dz, renal impairment, endocarditis, resternotomy or unwell pre-operatively
- Cardiac factors: unstable angina, LVEF < 30% (v poor), AMI < 90 days or systolic PAP > 60
- Surgical factors: emergency, non-CABG surgery, thoracic aorta or post-infarct septal rupture
Investigations:
FBE, UEC, coags, X-match
ECG
Echocardiogram – LVEF mild impairment 40-50%; severe impairment <30%
Coronary angiogram
CXR
How does off-pump CABG differ from an anaesthetic perspective?
Management is as for CABG but without bypass and using a ‘stabiliser’ to keep the heart as still as possible.
- Keep patient well filled with crystalloid.
- Keep patient warm (blood/fluid warmer, warming mattress/blanket, HME, etc.).
- May need vasoconstrictor when surgeon manipulates heart to maintain adequate BP.
- Consider TOE or oesophageal Doppler probe.
- Patient may still require full or half-dose heparin (surgical preference).
- If patient unstable, may need to go on bypass (1–10% of cases).
- For right/posterior descending coronary artery grafts, patient is placed in Trendelenburg position to increase venous return.
- Postoperatively: as for CABGs on bypass.
Indications for mechanical vs bioprosthetic valve replacements
mechanical valves in younger patients as they last longer but require anticoagulation
bioprosthetic valves only last 15 years but do not require anticoagulation.
Severity of aortic stenosis grading
Surface area
Mild: 1.6 - 2.5cm2
Mod: 1.0 - 1.5cm2
Severe: < 1.0 cm2
LV-aortic gradient
Mild < 20mmHg
Mod 20-50
Severe > 50
Haemodynamic goals for aortic stenosis valve surgery
Haemodynamic goals: fixed cardiac output, poorly tolerate ↓ SVR due to ↓ coronary perfusion → downward hypotensive spiral. May need infusions of vasopressor at induction.
PRELOAD ↑ NEED TO FILL NON-COMPLIANT VENTRICLE.
AFTERLOAD ↑ ADEQUATE DIASTOLIC BP TO MAINTAIN CORONARY PERFUSION.
CONTRACTILITY ↔
RATE ↔ AVOID EXTREMES. RAPID → ISCHEMIA. SLOW → ↓ CO.
RHYTHM SR CRITICAL FOR PRELOAD. ATRIAL KICK, NB FOR VENT. PRELOAD.
POST-CORRECTION SAME GOALS. VENTRICULAR HYPERTROPHY & DIASTOLIC DYSFUNCTION STILL VERY MUCH PRESENT.
Haemodynamic goals for aortic regurgitation and degree of severity
Full fast and forward
Severity determined on echo (jet width > 60% at cusp level = severe)
- *PRELOAD ↑** NEED ADEQUATE VENOUS FILLING.
- *AFTERLOAD ↓** TO PROMOTE FORWARD FLOW.
- *CONTRACTILITY ↔**
- *RATE ↑** –> ↑ CO & MAINTAIN SMALLER CHAMBER SIZE.
- *RHYTHM** NOT CRITICAL.
- *POST-CORRECTION** PERSISTENT MR, PHT, RV DYSFUNCTION.
Haemodyamic goals for mitral stenosis
PRELOAD ↔ MAINTAIN GRADIENT BUT AVOID PULMONARY OEDEMA.
AFTERLOAD ↓ RIGHT SIDE (AVOID HYPOXIA, HYPERCARBIA, ACIDOSIS).
CONTRACTILITY RV MAY NEED SUPPORT. LV USUALLY OK.
RATE ↓
RHYTHM USUALLY IN AF → CONTROL VENTRICULAR RESPONSE
IF IN SR, ONSET OF AF CAN PRECIPITATE DECOMPENSATION.
POST-CORRECTION RV SUPPORT IF SEVERE PULM. HYPERTENSION.
LV DYSFUNCTION MAY BE UNMASKED.
What is protamine, the dose for heparin reversal and its 5 adverse effects?
Protamine – a cationic base protein derived from salmon sperm Mechanism of action – cationic basic protamine combines with anionic acid heparin to form a stable complex devoid of anticoagulant activity.
Dose: 1mg per 100 IU heparin still circulating (within last 2 hrs) or 1.3mg/kg per 100 units heparin remaining as calculated from ACT
Time course: complexes cleared within 20 min by RES cf half life of heparin (90 min) allowing “rebound” heparin effect.
- *Anticoagulant effect** in the absence of heparin or protamine overdose
- *Histamine release** on rapid infusion (<5min) → hypotension
- *Pulmonary HTN**, oedema and bronchoconstriction: thromboxane and 5-HT-mediated pulmonary VC
- *Allergies** – if exposed to protamine insulin preparations, fish allergy → type I IgE-mediated anaphylaxis reaction
- *Heparin rebound** due to difference in t ½ (20 min vs 90min)
Haemodynamic goals for mitral regurgitation?
Full, fast and forward
Preload - euvolaemia
Afterload - decrease to reduce regurgitant fraction
Contractility - maintain
Rate - increase to reduce ventricular size
Rhythm - not critical
Post correction effectively increases LV afterload and can unmask LV dysfunction –> use an inodilator
Haemodynamic goals for cardiac tamponade
Preload - increase
Afterload - maintain with vasopressors
Contractility - maintain(CRITICAL)
Rate - increase as RATE dependent cardiac output
Rhythm - sinus tachy
Post-correction - rebound HTN so deepend anaesthesia and support as required
