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