Post on 20-Jun-2020
Dr Scott Minns ST5
Anaesthesia for patients with Cardiac Disease
There is a lot on the curriculum
What we’re going to cover today.. 01
Indications for cardiac surgeryRiskWho gets surgeryPerioperative management
02Valvular disease
Common valvular diseases
03Coronary artery diseaseCABGOn vs off pump
04Cardiac bypassComing on and off pump (separate talk on bypass machine)
05Wrap up
Who gets cardiac surgery?
● Common○ Coronary artery bypass graft○ Valvular heart disease○ Electrophysiology Ablations○ TAVI etc...
● Less common○ Pulmonary embolism○ Surgery on the thoracic aorta○ Congenital heart disease surgery
● Really rare○ Tumour○ Transplant○ LVAD
Specific-18 criteria.
Estimates risk of in-hospital death after cardiac surgery.
POSSuM
Goldman index (lee et al.) 0.5 (0)-9%(3) risk
Pick a scoring system for cardiac
risk and know it!
Risk Scoring
Variable weightings complex..
1. High risk surgery2. IHD3. HF4. Cerebrovascular disease5. T1DM6. CKD
Euroscore II
Scoring systems
Fatigue, dyspnoea and anginaI. No Sx on ordinary activity
II. Ordinary activity inducesIII. Minimal activity inducesIV. At rest
Angina I. On Exertion
II. Causing Slight limitationIII. Causing Marked limitationIV. At rest
NYHA heart failure Canadian Cardiovascular SocietyI. Poor < 4 mets Walking
indoorsII. Intermediate 4-7 mets
Walking 1-2 blocksIII. Good >7 mets
swimming
Dukes activity score
Investigations
Wall and valvular functionEJF is not a good indicator of
risk!Stress echo may be useful
Definitive information about arterial supply
ClinicalOne MET 3.5ml/kg/min
Four mets 1 flight of stairsNYHA 1-4
ECGIschemic
HypertrophicConduction abnormalities
Echo
Angio CPEXExplain CPEX?
Vo2 max 15ml O2 kg/minAT 11ml/kg/min
Biological markersBNP
Troponin
Anaesthesia for valve disease
RheumaticDegeneration and calcification
May be age related on congenital bicuspid
About 50% rheumaticFollowing rupture of chordae/papillary musclesValvular dilatation
Infectious (Rheumatic/Endocarditis)Congenital (Bicuspid)
Degenerative and tissue (eg marfans)Inflammatory (RA/SLE)
Aortic root dilatation
Almost always due to rheumatic fever post strep infection
VALVULAR DISEASE
Aortic Stenosis
Mitral StenosisMitral Incompetence
Aortic Incompetence
Aortic Stenosis -Fixed cardiac output state
Pathophysiology Peak pressure grad (mmHG)● Normal <5● Mild <25● Moderate 25-40● Severe >40
Implications for AnaesthesiaPreload - maintain to ensure flow across valve
Rate and rhythm - bradycardia decreases output but tachycardia limits diastolic perfusion time
Contractility- Avoid myocardial depression, risk of ischemia with aggressive inotropy and chronotropy
SVR - decreased SVR leads to poor coronary perfusion
Valve area (cm3)● Normal 2.5-3.5● Mild >1.5● Moderate 1-1.5● Severe 1.0● Critical <0.7
● As valve area narrows pressure in LV increases ● Concentric hypertrophy● Increased myocardial oxygen demands● Prolonged systole● High intramural pressures decrease coronary flow● Subendocardial ischemia● Loss of compliance leads to dependance on atrial filling
Full, slow, tight!
Aortic Incompetence
Pathophysiology
Implications for AnaesthesiaPreload - Normovolemia to ensure filling
Rate and rhythm - rapid rate decreases diastolic filling LVEDV decreased so less over distention
Contractility- Avoid myocardial depression
SVR - low to favour forward flow
● Typically chronic, acute tends to lead to decompensation and pulmonary oedema● Decreased forward blood flow with continuous volume overload● Eccentric hypertrophy with increased compliance● Initially on ascending part of Frank-starling curve as myofibrils over distend failure ensues● Regurgitant fraction >0.6 Severe● Increased compliance - increased vol for pressure - decrease in wall tension + O2 demand● EFF maintained as SV and LVEDV increase together
Fast, loose!
Mitral Stenosis
Pathophysiology
Implications for AnaesthesiaPreload - maintain to ensure flow if LAP falls CO will fall
Rate and rhythm - bradycardia increases stroke vol at expense of output. Tachycardia decreases SV+ CO. Aggressively manage AF
Contractility- Avoid myocardial depression
SVR - normal SVR ensures to coronary perfusion
Valve area (cm3)● Normal 4-6● Mild 1.6-2.5● Moderate 1.1-1.5● Severe <1.0
● As stenosis increases LA dilates and hypertrophies● Atrial contraction contributes greater amounts to filling● Bradycardia allows sufficient time for flow across valve● As stenosis progresses leads to pulmonary hypertension
and RV overload● Exercise tolerance good disease guide
Full, slow, tight!
PVR - hypercapnia, hypoxia, acidosis, nitrous will increase PVR
Mitral Incompetence
Pathophysiology
Implications for AnaesthesiaPreload - avoid large increases in preload as will further distend LA
Rate and rhythm - Relative tachycardia
Contractility- avoid myocardial depression
SVR - forward flow dependant on low SVR
● Regurgitant flow back into left atrium >#0.6 Severe● LA and LV overload● Usually well preserved function of LV as blood ejected through Mitral and Aortic valve● In time leads to poor contractile function● LA dilates but AF not so critical● Rapid heart rate allows for compensation -decreased time for overload● Bradycardia may cause further dilatation of the annulus and worsen incompetence
Full, Fast, Loose!
Cardiac disease in pregnancy
Time for a question?
Anaesthesia for CABG
Blood supply to the heart
Arterial supply
● Right supplies○ RV, RA part of the interventricular
septum○ The SAN in 65%○ AVN and conducting system 80%
● Left supplies○ LA, LV, part of the septum SAN in 35%○ AVN and conducting system 20%
● Innermost endocardium receives O2 directly
Venous drainage
● 1/3 direct into chambers via venae cordi minimae● Remainder by veins that accompany coronary
arteries into RA
KEY NUMBERS
∼250 ml/min or 5% of CO
Ischemia occurs when demand outstrips supply
Resting coronary blood flow is:
Arterial oxygen extraction is 70–80%
so increased requirements must be met with increased supply
Who gets CABG/when
Indications for CABG (American College of Cardiology (ACC) and the American Heart Association (AHA)) are:
● > 50% left main coronary artery stenosis● > 70% stenosis of the proximal left anterior descending (LAD) and proximal circumflex arteries
● Three-vessel disease in asymptomatic patients or those with mild or stable angina● Three-vessel disease with proximal LAD stenosis in patients with poor left ventricular (LV) function
● One- or two-Vessel disease and a large area of viable myocardium in high-risk area in patients with stable angina● Over 70% proximal LAD stenosis with either an ejection fraction (EF) below 50% or demonstrable ischemia
Blood supply to the heart
Control of blood supply
● Flow is governed by driving pressure ○ crucial in presence of stenosis
● Vasodilatation in response to local metabolites● Autonomic control present but negligible
● During systole subendocardial pressure exceeds coronary artery pressure○ Left heartflow in diastole (some in systole in outer areas)○ Right heart throughout
● High HR can compromise perfusion and filling
● Supply is dependent on blood flow, O2 content and R/L shift of oxyhemoglobin curve● Demand is dependant on afterload, preload, contractility and rate
● Decreased risk of CVA● Permits earlier extubation● Decreased length of stay● Less disruption to coagulation
○ Less blood products● LAD graft does not necessarily
require sternotomy
● Increased hemodynamic instability● Risk of myocardial ischemia● Not suitable for all patients/vessels
eg diffuse or severe disease● ?Higher mortality
Coronary artery bypass grafting on vs off pump
Advantages Disadvantages
● Hemodynamic instability on lifting the heart● To work on lateral/posterior aspects
○ Verticalisation causes regurgitation● External compression● Minimised with
○ MAP >70○ Avoid tachycardia to decrease O2 demand
● Preemptive occlusion of target vessel for 5min followed by 3 min of reperfusion help to preserve ATP concentration.
Ischemic preconditioning
Cardiac● MI● Graft Kink● Valve failure● Arrhythmia● Tamponard● Cardiac failure
Circulatory● SIRS/SEPSIS● Vasoplegia● Hypovolemia/Hemorrhage
Respiratory● Tension pneumothorax● Pulmonary hypertension
Anaesthetic● Excess sedation/nitrates● High ventilation
pressures
Anaesthetic● Inadequate sedation● Inadequate Analgesia● Residual NMB
Respiratory● Hypoxia ● Hypercarbia
Other● Excess vasoconstriction● Excess ionotropy● LVH● Raised ICP● Bladder distention
Common post op complications
Hypotension Hypertension
Intraop ● CVA secondary to
hypoperfusion/embolic● ICH
Post op● CVA secondary to AF● Delerium● Ischemic optic neuropathy
Brachial plexus injury● traction/compression
Phrenic nerve palsy● Ice flush
Anterior intercostal nerve● thoracic artery
harvesting
Neurological complications
Central Peripheral
Risk factors● Patient
○ Age, Male, LV dysfunction, Lv thrombus (TOE), Prior stroke, carotid stenosis, DM, AF, renal failure
● Procedure○ Long CPB, Valve surgery, hyperglycemia, poor temperature control, cerebral
hypoperfusion, inadequate anticoagulation
Minimising risks ● ACT >400, CPB filters, CPB <2hrs, Off pump, Temp/BP/acid base/glycemic control
The basics
Cardiopulmonary bypass
Cardiopulmonary bypass basics
Cardioplegia Hypothermia
Starting bypass Weaning bypass
Acid base correction Anticoagulation
Allows surgery in a motionless bloodless fieldVenous blood is drained oxygenated and returned
Starting bypass
Handover to perfusionAnaesthesia targetsVasoactive agents
Arterial inflowOxygenated blood supply
Risks of malposition and dissection
Good outflow imperativeRisks of svc obstruction
Venous drainage
Pulsatile flow Inadequate supply
Injury to RBCPlatelet, leukocyte and fat re
transfusion
Adequate bypass
Drugs and ventilation
Cardioplegia
Cardioplegia● Diastolic electromechanical arrest● Aims
○ Combats ion loss○ Buffers ischemic acidosis○ Decreases O2 consumption and prolonges ischemic time
● It is a○ Hyperkalemic solution○ Hyperosmoitic to prevent tissue oedema○ Alkalotic to attenuate pH change○ Low Ca2+ to decrease contractility○ Aspartate and glutamine (promotes oxidative metabolism
● May be given ○ Anteriorgrade - into direction of flow, in aortic root/ostium○ Retrograde (may not protect R/V) into R coronary sinus
● May cause
○ MI, dysrhythmia -VF on administration● Underdosing -moving field● Hyperkalemia● Ischemic and reperfusion injuries.
Decreased cerebral metabolic demand
● Cerebral protection● Decreased microemboli● Decreased BBB
permeability● Decreased axonal death
Decreased systemic O2 demand● decreased myocardial
demand
Decreases inflammatory response
● CPB is pro inflammatory
Increased blood viscosity● increased VTE risk
Increased infection rate● Impaired wound healing● immunosuppression
Peripheral vasoconstriction
Hypothermia
Advantages Disadvantages
Left shift of oxyhemoglobin dissociation curve
Heparin
AnticoagulationAnother time!
Weaning bypass
De-airingContractility
FillingValve function
Restart
TemperatureRe-warmed
36-37OC
Rate/Rhythm/ContractilityEpicardial pacing
Consider vasoactive/inotropic requirements
TOE
Ventilation Lines outClamped and removed
Stability is important for vessel closure
BiochemistryElectrolytesOxygenation
Protamine
CONCLUSIONSThere is lots to know!
Hopefully you have a better understanding of surgery for valve
disease, bypass and CABG
We haven’t covered:Anticoagulation, heparin, protamine,
ACT, TEGPH-Stat va Alpha-stat
Inotropes, Ionodilators, Vasodilators and Vasopressors
Pulmonary hypertensionThe Transplanted Heart
Cardiology (ECG, Rhythm, MI, pacemakers)
Does anyone have any questions?
THANKS