ABA Cardiac Anesth cheat sheet

Determinants of myocardial oxygen consumption (MVO2) are heart rate, contractility, and wall stress; heart rate and systolic wall stress dominate, so tachycardia and left ventricular dilation are especially costly.

Coronary perfusion pressure = aortic diastolic pressure minus left ventricular end-diastolic pressure; coronary flow is predominantly diastolic, so tachycardia and elevated LVEDP both promote subendocardial ischemia.

Left ventricular pressure-volume loop: filling, isovolumic contraction, ejection, isovolumic relaxation; the end-systolic pressure-volume relationship slope (Ees) is a load-independent contractility index and arterial elastance (Ea) approximates afterload.

Frank-Starling relationship: stroke volume rises with preload up to optimal sarcomere length; a dilated failing ventricle has a flatter curve and is more dependent on afterload reduction than on volume loading.

Laplace law: wall stress = (pressure x radius) / (2 x wall thickness); dilation raises wall stress and MVO2, whereas hypertrophy normalizes stress at the cost of impaired diastolic filling.

Volatile anesthetics cause dose-dependent decreases in mean arterial pressure, systemic vascular resistance, and contractility; sevoflurane is acceptable for inhalational induction, and isoflurane-induced coronary steal is not clinically established.

Etomidate preserves hemodynamics but even a single induction dose inhibits 11-beta-hydroxylase and suppresses cortisol for 24-48 hours; propofol causes vasodilation and negative inotropy, and ketamine raises sympathetic tone despite direct negative inotropy.

Receptor effects: beta-1 produces inotropy and chronotropy, beta-2 produces vasodilation and bronchodilation, alpha-1 produces vasoconstriction, and M2 activation produces bradycardia; adenosine causes coronary vasodilation and atrioventricular block.

Common vasoactive doses: phenylephrine 40-100 mcg bolus (alpha-1); norepinephrine 0.01-0.2 mcg/kg/min; epinephrine 0.01-0.1 mcg/kg/min; dobutamine 2-20 mcg/kg/min (beta-1); milrinone 0.375-0.75 mcg/kg/min (PDE3 inhibitor); vasopressin 0.01-0.04 units/min (V1).

The STS predicted risk of mortality and EuroSCORE II are standard cardiac surgical risk tools; the STS model includes age, renal dysfunction, ejection fraction, reoperation, urgency, and procedure type.

For noncardiac surgery, the Revised Cardiac Risk Index uses six factors: ischemic heart disease, heart failure, cerebrovascular disease, insulin-treated diabetes, creatinine greater than 2 mg/dL, and high-risk surgery.

ACC/AHA stepwise approach: emergency surgery proceeds without delay; active cardiac conditions (unstable angina, decompensated heart failure, severe arrhythmia, severe valve disease) require evaluation; functional capacity of at least 4 METs usually permits surgery without stress testing.

Do not start beta-blockers on the day of surgery; continue chronic therapy, and if initiation is planned, begin days to weeks before surgery with titration to heart rate and blood pressure.

Antiplatelet management: continue aspirin through cardiac surgery when possible; stop clopidogrel 5 days, ticagrelor 3-5 days, and prasugrel 7 days before elective surgery to limit bleeding.

Warfarin: stop about 5 days preoperatively; bridge with low-molecular-weight heparin only for high thrombotic risk such as a mechanical mitral valve, recent stroke, or atrial fibrillation with prior embolism; direct oral anticoagulants are stopped 48-72 hours depending on renal function and bleeding risk.

Preoperative echocardiography quantifies ejection fraction, valve lesion severity, and pulmonary pressures; stress testing is indicated when results would change management, and coronary angiography is reserved for symptomatic or high-risk patients.

Preoperative anemia and iron deficiency independently predict worse outcomes; restrictive transfusion (hemoglobin 7-8 g/dL) is generally preferred, with a higher threshold during active myocardial ischemia.

Frailty, cognitive impairment, and malnutrition are independent risk factors and should be included in the preoperative assessment and shared decision-making discussion.

Standard monitoring includes a 5-lead ECG with leads II and V5 for ST analysis, pulse oximetry, capnography, and temperature; place an arterial line before induction in high-risk patients or when vasoactive infusions are planned.

Central venous pressure correlates poorly with volume responsiveness; dynamic indices (pulse pressure variation or stroke volume variation greater than 13%) and echocardiographic assessment are more reliable in ventilated patients with sinus rhythm.

Fick principle: cardiac output = oxygen consumption / (arterial oxygen content minus venous oxygen content); thermodilution and pulse-contour analysis provide continuous estimates, and mixed venous saturation below 65% suggests inadequate oxygen delivery.

TEE views: midesophageal four-chamber at 0-20 degrees, midesophageal long-axis at 120-140 degrees, and transgastric midpapillary short axis for left ventricular function and volume; Doppler estimates gradients and cardiac output.

TEE contraindications include esophageal stricture or tumor, perforated viscus, active gastrointestinal bleeding, and recent esophageal or gastric surgery; complications include odynophagia, dental injury, esophageal perforation, and bacteremia.

Cardiac tamponade: right atrial systolic collapse, right ventricular diastolic collapse, inferior vena cava plethora, and greater than 25-30% respiratory variation in mitral inflow; pulsus paradoxus greater than 10 mmHg is a clinical clue.

Severe aortic stenosis: mean gradient at least 40 mmHg, peak velocity at least 4 m/s, valve area at most 1.0 cm2; avoid tachycardia and hypotension because coronary perfusion depends on diastolic pressure.

Right ventricular failure: elevated central venous pressure, low mixed venous saturation, clear lungs, and echocardiographic dilation; treat with inhaled pulmonary vasodilators and inotropes while avoiding hypoxia, hypercapnia, and high airway pressures.

CPB components: venous reservoir, roller or centrifugal pump, membrane oxygenator with heat exchanger, arterial filter, and cardioplegia delivery system; priming volume of roughly 1.5-2 L produces hemodilution.

Anticoagulation: heparin 300-400 units/kg to achieve an activated clotting time above 400-480 seconds; recheck the ACT every 30 minutes; protamine 1 mg per 100 units of heparin, given slowly to avoid hypotension and pulmonary vasoconstriction.

Target pump flow 2.0-2.4 L/min/m2, mean arterial pressure 50-80 mmHg, and hematocrit above 20-25% on bypass; oxygen delivery = cardiac output x arterial oxygen content x 10, guided by lactate and mixed venous saturation.

Cardioplegia: cold blood cardioplegia at a 4:1 ratio with potassium 15-30 mEq/L; antegrade via the aortic root, retrograde via the coronary sinus; del Nido solution allows single dosing for up to 90 minutes.

Hypotension on CPB: check pump flow, venous return, arterial line damping, anesthetic depth, and vasodilation; treat with vasopressors or flow adjustment and exclude aortic dissection and cannula malposition.

Intra-aortic balloon pump: inflates in diastole and deflates at end-diastole, augmenting coronary and systemic perfusion while reducing afterload; contraindicated in aortic regurgitation and aortic dissection.

VA-ECMO provides respiratory and circulatory support; retrograde aortic flow increases left ventricular afterload, so venting is required in severe left ventricular dysfunction, and differential hypoxia (harlequin syndrome) can occur with femoral cannulation.

Continuous-flow LVAD: axial or centrifugal pump; target mean arterial pressure 65-80 mmHg; key complications are pump thrombosis, acquired von Willebrand bleeding, and right heart failure.

Hypothermic circulatory arrest is typically conducted at 18 degrees C with cerebral protection for aortic arch reconstruction.

Postoperative bleeding: output greater than 200 mL/hour for 2 consecutive hours or greater than 400 mL in the first hour warrants checking ACT, platelets, fibrinogen, and viscoelastic testing (TEG/ROTEM) and considering reexploration.

Transfusion triggers: platelets below 50 x 10^9/L, fibrinogen below 150-200 mg/dL, or prolonged INR with active bleeding; target hemoglobin 7-8 g/dL unless there is active myocardial ischemia.

Low cardiac output syndrome: cardiac index below 2.0-2.2 L/min/m2 with hypotension, oliguria, cool extremities, and rising lactate; treat with inotropes, vasodilators, mechanical support, and correction of ischemia or tamponade.

Vasoplegia after bypass: low systemic vascular resistance with normal or high cardiac output; use norepinephrine, vasopressin, and methylene blue after excluding bleeding, tamponade, and pump failure.

Postoperative atrial fibrillation occurs in 20-40% of patients; beta-blockers reduce incidence, amiodarone is used for rhythm control, and potassium, magnesium, and precipitating causes should be corrected.

Early extubation within 6 hours is facilitated by multimodal analgesia, normothermia, minimal bleeding, and stable hemodynamics; delirium screening and early mobility reduce complications.

Renal protection: maintain perfusion pressure and avoid nephrotoxins; acute kidney injury after cardiac surgery is common and associated with increased mortality, and dialysis is indicated for refractory hyperkalemia, acidosis, or volume overload.

Glycemic control with an insulin infusion targeting below 180 mg/dL while avoiding hypoglycemia; stroke occurs in 1-5% of patients and is diagnosed with CT or MRI and managed supportively.

Shunt physiology: a pulmonary-to-systemic flow ratio above 1 indicates a left-to-right shunt; rises in pulmonary vascular resistance or falls in systemic vascular resistance can reverse the shunt and cause cyanosis, so air bubbles in intravenous lines must be excluded.

Eisenmenger syndrome: irreversible pulmonary vascular disease with right-to-left shunt; systemic vasodilation, hypoxia, and acidosis worsen cyanosis, so pulmonary vasodilators are used and dehydration is avoided.

Fontan circulation: passive cavopulmonary flow, so cardiac output depends on low pulmonary vascular resistance; hypoxia, hypercapnia, high airway pressures, and hypovolemia are poorly tolerated, and a fenestration permits right-to-left decompression.

Heart transplantation: the donor heart is denervated, so atropine is ineffective; isoproterenol or direct-acting chronotropes are used, and acute rejection and graft dysfunction are monitored early.

Lung transplantation: one-lung ventilation and ECMO may be required; primary graft dysfunction presents as hypoxemia and pulmonary edema within the first 72 hours.

One-lung ventilation hypoxemia: use lung-protective tidal volumes, PEEP to the dependent lung, CPAP to the non-ventilated lung, and fiberoptic bronchoscopy to correct tube malposition.

Carcinoid syndrome: avoid histamine-releasing drugs and catecholamines; octreotide 50-100 mcg intravenously treats crisis, and vasoplegia or bronchospasm may occur during tumor manipulation.

Pulmonary hypertension: inhaled nitric oxide, epoprostenol, and sildenafil reduce pulmonary vascular resistance; avoid systemic hypotension and acidosis, and note that abrupt nitric oxide withdrawal can cause rebound pulmonary hypertension.

Electrophysiology procedures: pacemaker and ICD lead extraction carries risk of tamponade and vascular injury, so general anesthesia with TEE and arterial monitoring is commonly used.

WHO Surgical Safety Checklist: sign in, time out, and sign out; it improves team communication and reduces complications, and cardiac versions add items for TEE, bypass, and anticoagulation.

Closed-loop communication and structured handoffs (SBAR) reduce information loss at ICU transfer, and read-back of verbal orders prevents medication errors.

Central line bundle: hand hygiene, maximal sterile barrier, chlorhexidine antisepsis, optimal site selection, and daily review of line necessity; together these reduce catheter-related bloodstream infections.

Surgical antibiotic prophylaxis is given within 60 minutes before incision (120 minutes for vancomycin and fluoroquinolones), redosed according to half-life and blood loss, with normothermia and normoglycemia maintained.

Morbidity and mortality conference: confidential, nonpunitive review of complications that supports system improvement and individual learning; just-culture principles distinguish human error from reckless behavior.

Crew resource management: assertiveness, situational awareness, and a flattened hierarchy improve safety, and simulation with debriefing improves team performance.

Never events such as wrong-site surgery, retained foreign bodies, and wrong-blood transfusion are reportable; root cause analysis identifies system failures rather than blaming individuals.

Professionalism obligations include informed consent, capacity assessment, conflict-of-interest disclosure, and appropriate supervision of trainees.

Quality metrics include STS database outcomes, risk-adjusted mortality, prolonged ventilation, renal failure, and reexploration, which support public reporting and pay-for-performance programs.

Determinants of myocardial oxygen consumption (MVO2) are heart rate, contractility, and wall stress; heart rate and systolic wall stress dominate, so tachycardia and left ventricular dilation are especially costly.

Coronary perfusion pressure = aortic diastolic pressure minus left ventricular end-diastolic pressure; coronary flow is predominantly diastolic, so tachycardia and elevated LVEDP both promote subendocardial ischemia.

Left ventricular pressure-volume loop: filling, isovolumic contraction, ejection, isovolumic relaxation; the end-systolic pressure-volume relationship slope (Ees) is a load-independent contractility index and arterial elastance (Ea) approximates afterload.

Frank-Starling relationship: stroke volume rises with preload up to optimal sarcomere length; a dilated failing ventricle has a flatter curve and is more dependent on afterload reduction than on volume loading.

Laplace law: wall stress = (pressure x radius) / (2 x wall thickness); dilation raises wall stress and MVO2, whereas hypertrophy normalizes stress at the cost of impaired diastolic filling.

Volatile anesthetics cause dose-dependent decreases in mean arterial pressure, systemic vascular resistance, and contractility; sevoflurane is acceptable for inhalational induction, and isoflurane-induced coronary steal is not clinically established.

Etomidate preserves hemodynamics but even a single induction dose inhibits 11-beta-hydroxylase and suppresses cortisol for 24-48 hours; propofol causes vasodilation and negative inotropy, and ketamine raises sympathetic tone despite direct negative inotropy.

Receptor effects: beta-1 produces inotropy and chronotropy, beta-2 produces vasodilation and bronchodilation, alpha-1 produces vasoconstriction, and M2 activation produces bradycardia; adenosine causes coronary vasodilation and atrioventricular block.

Common vasoactive doses: phenylephrine 40-100 mcg bolus (alpha-1); norepinephrine 0.01-0.2 mcg/kg/min; epinephrine 0.01-0.1 mcg/kg/min; dobutamine 2-20 mcg/kg/min (beta-1); milrinone 0.375-0.75 mcg/kg/min (PDE3 inhibitor); vasopressin 0.01-0.04 units/min (V1).