Cardiothoracics Flashcards
Types of cardiomyopathy and how it affects CO, SV, contractility
- Dilated
- low CO, SV and contractility - Hypertrophic
- low CO + SV, high contractility - Restricted
- normal/low CO, low SV, normal contractility
Causes of dilated cardiomyopathy
- Idiopathic
- Ischaemic
- Valvular
- Post-viral
- Peri/post-partum
- Post-chemotherapy
- Sickle cell disease
- Alcohol
- Hypothyroid
- Muscular dystrophy
Pre-assessment DCM
- Baseline ECG
- U&Es if on ACEI
- FBC
- ECHO if not up to date
- Consider CXR
- Sometimes dobutamine stress test
Indications for pre-assessment ECHO
- High risk surgery e.g. open AAA, peripheral vascular surgery
- Ventricular function concerns
- dyspnoea suspected cardiac
- IHD with poor functional capacity
- Known cardiac failure, no ECHO in last 2 years
- Known cardiac failure, worsening symptoms - Valvular concerns
- Undiagnosed systolic murmur
- Significant valvular disease, no ECHO in last 2 years
- Moderate/severe AS, no ECHO in last 1 year
- Valve disease or replacement with worsening symptoms
- Bioprosthetic valve replacement, no ECHO in 5 years
30 day cardiac event rates for non-cardiac surgery
Minor <1%
- breast, dental, endocrine, eye, minor gynae, reconstructive, minor ortho e.g. knee, minor urology
Intermediate 1-5%
- abdominal incl. major gynae, carotid, peripheral arterial angioplasty, endovascular AAA, head and neck, major ortho e.g. hip/spine, major urology
High >5%
- open AAA, peripheral vascular surgery
Medical management of DCM
RAAS inibition (ACEI or ARB if not tolerated)
- Reduced dyspnoea, improved ET
- Reduced hospital stay
- Slow disease progression
- Reduced mortality
** Beta blockers**
- Reduced mortality
Aldosterone inhibitors (spironolactone, eplenerone)
- Reduced mortality
Atrial naturetic peptides
- IV administration only
- Diuresis, naturesis, vasodilation
Anticoagulants if EF< 30%
SGLT-2 inhibitors
- Reduced mortality
Angiotensin nepriolysin inhibitors e.g. sacubitril-valsartan
- Inhibits breakdown of ANP, ACEI prevents side effect of vasoconstriction
Risks of DCM perioperatively
- Arrythmia
- Embolic events
- Congestive heart failure
- Death
Monitoring used intraoperatively for patient with DCM
AAGBI:
- NIBP, temp, SpO2, iCO2, etCO2, expired volatiles, 3-lead ECG, PNS
In addition:
- 5 lead ECG, IABP, CO monitoring
- BIS to titrate anaesthetic agents
- Consider TOE/oesophageal doppler
- Central venous pressures (preload)
How to manage cardiovascular physiology in DCM
- Avoid tachycardia (LV coronary arteries perfused during diastole)
- Maintain sinus rhythm and treat arrhythmias (reliance of atrial contraction for filling)
- Maintain blood pressure (diastolic pressure perfuses LV coronary arteries)
- Avoid rise in SVR e.g. with ketamine (afterload=LV chamber pressure + SVR, already higher in DCM), but also avoid precipitous drop (diastolic pressures perfuse LV coronary arteries)
- Maintain normovolaemia/preload
- Correct electrolytes
- Avoid negative inotropy (provide ionotropic support if required -> PDEI, levosimendan, dobutamine N.B propofol and volatiles cause myocardial suppression)
Post operative management of surgery in pt with DCM
HDU/ITU setting for haemodynamic monitoring and management
Adequate analgesia to avoid increased SVR
Predictors of poor outcome in DCM
- LVEF <20%
- Elevated LVEDP
- Left ventricle hypokinesia
- Non-sustained VT
Pros and Cons of neuraxial block for DCM physiology
Pros:
- reduces SVR
- effective pain control avoids tachycardia
Cons:
- can cause drop in BP so reduced coronary artery perfusion
- treatment of hypotension with fluids risks pulmonary oedema
Non pharmacological treatment of DCM
- Partial left ventriculectomy
- Cardiac resynchronization pacing therapy
- Implantable cardiac defibrillator
- Left ventricular assist device (bridging to transplant)
- Heart transplant
Anaesthetic options in DCM
And haemodynamic goals
- Local - minimal haemodynamic changes, but stress can cause tachycardia and increased SVR
- Neuraxial - reduces afterload so improves cardiac output but risks hypotension and poor LV coronary artery perfusion
- GA - least stress response, asleep patient so easier to provide more invasive monitoring, airway control in event of critical incident but many agents cause negative inotropy. Give slow IV induction with increased opioid component and balanced maintenance (pEEG) if GA.
Aims:
Avoid tachycardia/rise in SVR + afterload
Avoid myocardial depression/negative inotropy
Maintain adequate preload
Prevent increases in afterload
Maintain sinus rhythm
Pathophysiology of HCM
Extracellular fibrosis-> hypertrophy, ventricular stiffness, shape distortion and diastolic impairment with preserved systolic function.
End stage: biventricular systolic dysfunction
Presentation of HCM
- Autosomal dominant so through genetic testing
- Angina
- Heart failure (dyspnoea, syncope, arrhythmia commonly AF)
- CVA
- Sudden death
Risk factors for sudden cardiac death in HCM
- Previous cardiac arrest
- FH sudden cardiac death
- previous VT
- Syncope
- Abnormal blood pressure response to exercise
- LV wall thickness >30mm
Medical management HCM
- Beta blockade (reduces heart rate, prolongs diastole, improves ventriclar filling) - > disopyramide as alternative
- Amiodarone to treat SVT/VT
Non-medical management HCM
- ICD
- Alcohol septal ablation
- Surgical myomectomy
Perioperative aims in HCM
- Adequate preload + afterload
- Maintain SVR
- Avoid sympathetic activation and tachycardia
- Reduce contractility
- Maintain sinus rhythm
- If hypotension with LVOTO, give fluid bolus and alpha-adrenergic agonist e.g. phenylephrine
Spinal causes decreased preload and afterload which can be dangerous - GA is preferred
Indications for endoscopic thoracic sympathectomy
Hyperhydrosis - palms, axilla, head and face
Chronic pain/upper limb regional pain syndrome
Facial blushing
Describe the sympathetic nerve supply to the upper limb
Preganglionic fibres from T1-T5 synapse in the superior, middle and inferior cervical ganglia
- post ganglionic fibres travel to effector cells
Implications of managing a patient for endoscopic thoracic sympathectomy under general anaesthesia
- Rare conversion to open thoracotomy (prep as if thoracotomy)
- Risk of major haemorrhage (ensure large bore IV access and G+S)
- Periods of hypoxia are common due to shunt, atelectasis and fairlure to fully inflate first lung before proceeding with surgery on second side (preoperative assessment of ability to tolerate this e.g. cardiovascular health)
- Hypotension due to capnothorax can happen (consider invasive blood pressure monitoring)
Complications due to patient positioning for endoscopic thoracic sympathectomy
Supine, reverse trendelenburg, arms abducted: brachial plexus injury
Prone: eye damage, dislodged airway, facial damage
Lateral: damage to pressure points e.g. peroneal nerve
Causes of restrictive cardiomyopathy
- Idiopathic
- Amyloidosis
- Sarcoidosis
- Haemochromatosis
- IHD
- HTN
- Valve disease
Pathophysiology restrictive cardiomyopathy
Impaired ventricular diastolic function due to fibrotic/infiltrative changes to myocardium and subendocardium
Symptoms restrictive cardiomyopathy
- Dyspnoea
- Fatigue
- Orthopnoea
- Palpitations
- Chest pain
Signs restrictive cardiomyopathy
- 3rd heart sound
- Raised JVP
- Ascites
- Oedema
- Systolic murmur
Medical treatment restrictive cardiomyopathy
- Beta blockers, CCBs
- Diuretics
- Maintain sinus rhythm (amiodarone, digoxin, beta blockers)
PPM/ICD in advanced conducting system dysfunction
Perioperative aims with restrictive cardiomyopathy
- Maintain adequate preload
- Maintain SVR
- Maintain sinus rhythm
- Minimise myocardial suppression (Can use ketamine)
Arrhythmogenic right ventricle cardiomyopathy pathogenesis, presentation, management
Pathogenesis: adipose and fibrous tissue replaces myocradial cells, re-entry circuits can form, RV becomes thin and dilated
Presentation: arrythmia, syncope, cardiac arrest, sudden death
Management: sotalol/verapamil/amiodarone for arrhthmia, Holter monitoring, catheter ablation as palliative, early ICD can be life saving
Options for airway management for endoscopic thoracic sympathectomy
- One lung ventilation via double lumen tube
- One lung ventilation via endotracheal tube with bronchial blocker
- Endotracheal tube with intrathoracic CO2 insufflation
- LMA with intrathoracic CO2 insufflation
Intraoperative complications during endoscopic thoracic sympathectomy
- Malposition of DLT or bronchial blocker = hypoxia
- One lung ventilation shunt = hypoxia (can be worsened by CPAP or oxygen insufflation to deflated lung reduces hypoxic pulmonary vasoconstriction, PEEP to inflated lung increases resistance to blood flow)
- Atelectasis of re-inflated lung may cause hypoxia in bilateral surgery
- Hypotension due to capnothorax
- Cardiac arrythmia due to intrathoracic diathermy
- Severe sleeding due to blood vessel damage during port insertion
Post-operative complications following endoscopic thoracic sympathectomy
- Ongoing hypoxia due to atelectasis and residual pneumothorax
- Risk of ALI if protective one-lung ventilation not used
- Chest pain
- Compensatory hyperhidrosis
Which vessels are commonly harvested for CABG
Saphenous vein
Internal mammary artery
Radial artery
List advantages of “off-pump” CABG vs “on bypass” CABG
- Reduced platelet dysfunction
- Reduced consumption of clotting factors
- Reduced inappropriate fibrinolysis
- Reduced risk of blood transfusion (because reduction in above coagulation defects)
- Reduced renal dysfunction
- Reduced risk fluid overload/depletion
- Reduced risk electrolyte distrubance
- Reduced risk SIRS
- Reduced risk air emboli
- Reduced risk direct aorta damage
- Reduced risk neurological dysfunction
- Reduced hypothermia
- Earlier extubation
- No ICU stay
- Reduced morbidity/mortality
Causes of haemodynamic instability in “off-pump” CABG
- Ischaemia due to vessel anastomosis
- Mechanical displacement of heart
- Impaired cardiac filling due to immobilisation device
- Arrythmias
- Bleeding
List strategies which can help to minimise haemodynamic instability during “off-pump” CABG
- Minimise heart manipulation
- MInimise periods of ischaemia
- Keep heart rate normal-low
- Monitor and treat electrolyte disturbances
- Ensure patient is adequately filled
- Good communication between anaesthetist and surgeon
Methods to minimise hypothermia during “off-pump” CABG
- Ensure patient temperature is normal before starting
- Minimise periods of leaving patient unconvered
- Warmed intravenous fluids
- Forced air warming blanket
- Under body resistive heating mat
- Raise ambient theatre temperature to a minimum of 21 degrees celcius
- Foil hat
List indications for one lung ventilation
Absolute:
* Isolation of diseased lung to prevent contamination of healthy lung e.g. haemorrhage, empyema
* Control distrubution of ventilation e.g. bronchopleural fistula, major bulla
* VATS
Relative:
* Thoracic surgery
* Thoracic aortic aneurysm
* Oesophagectomy
* Mediastinal mass surgery
* Minimally invasive cardiac surgery
Give specific indications for placement of a right sided double lumen tube
- Surgery that involves the left main bronchus e.g. left pneumonectomy
- Distortion of the left main bronchus anatomy e.g. tumour compressing left main bronchus
List disadvantages of using a double lumen tube for one lung ventilation
- Larger and more rigid tube so increased risk of airway and oral trauma
- More difficult to insert in patients with difficult airway
- May need to exchange for single lumen at end of case if post-operative ventilation required
- Tube can become dislodged and so fail to isolate one lung
How can the risks associated with lung resection be quantified preoperatively?
- Lung function tests e.g. predicted post-operative FEV1 and DLCO based on anatomic calculation, V/Q scans or CT evaluation - (FEV>1.5 or post-op FEV1 and DLCO >40%)
- Higher risk patients may warrant functional assessment e.g. CPET (peak VO2 most useful)
- Mortality risk prediction scores e.g. RESECT-90, thoracoscore
- Cardiac risk prediction e.g. Thoracic Revised Cardiac Risk Index
- Assessment of pre-existing pulmonary hypertension with ECHO
List the steps that may improve hypoxaemia resulting from one lung ventilation
General:
* Call for help
* Increase FiO2
* Alert theatre team
* A-E assessment
Specific:
Quick checks
* Reconfirm position of DLT using fibroptic scope, assess for obstruction in tube e.g. mucus plug
* Ensure haemodynamics and cardiac output optimised, ensure no major haemorrhage, correct Hb
Optimise ventilated lung:
* Recruitment manouevre to ventilated lung
* Increase PEEP to ventilated lung (recuit alveoli, but may impair blood flow causing shunt)
* If pneumonectomy, clamp pulmonary artery to non-ventilated lung
* Consider TIVA (volatiles impair hypoxic vasoconstriction to non-ventilated lung)
Optimise non ventilated lung
* Apply CPAP 1-5cmH2O to non ventilated lung
* Intermittent reinflation of non-ventilated lung
* Severe desaturation: resume bilateral ventilation
Options to maintain anaesthesia for rigid bronchoscopy
Volatile: connect anaesthetic circuit to side port of bronchoscope (intermittent delivery, unreliable but bronchodilation and familiarity)
TIVA: more reliable, more familar now, requires pEEG and is more expensive
Options to manage gas exchange during rigid bronchoscopy
High-flow apnoeic oxygen with leak to avoid baro/volutrauma
High-frequency automated jet ventilation e.g. Monsoon
Manual low-frequency jet ventilation e.g. Sander’s
Controlled ventilation via anaesthetic circuit attached to 22mm side port
Pros and cons of HFJV
Pros:
* Less haemodynamic compromise than conventional PEEP
* Minimal movement of vocal cords/surgical field
* Improved surgical access
* Versatile
* Less ADH production and fluid retention than PPV
Cons:
* Risk of barotrauma
* Air is cool and dry
* etCO2 monitoring is unreliable
* Increased dead-space
* Volatiles are impractical (and contaminate theatre environment)
List laser specific patient safety considerations
- Maintain FiO2 <40%
- Do not use nitrous oxide
- Saline-soaked gauze over mouth, teeth and in airway
- Ensure goggles for patient (and theatre staff)
- Is tube, use laser tube
- Equipment used should be laser compatible
List laser specific safety considerations for theatre (not patient)
- Goggles for staff
- Signs on doors
- Theatre doors locked
- Blinds down
- Laser trained staff members to operate laser
- Equipment maintenance
List anaesthetic complications of rigid bronchoscopy
- Barotrauma
- Awareness
- Inadequate gas exchange
- Laryngospasm, bronchospasm
- Impaired venous retrun (from high intrathoracic pressures)
- Dysrhthmia from jet ventilation
- Airway contamination
Surgical complications of rigid bronchoscopy
- Soft tissue trauma e.g. lips, tongue, vocal chords
- Dental damage
- Major haemorrhage
- Pneumothorax
- Cervical spine damage
What are the purposes of cardioplegia?
- Reduce oxygen demand of the heart
- Reduce ischaemic effects of bypass
- Still heart for surgery
- Bloodless field
What is the typical composition of cardioplegic solution?
- High potassium concentration approx 20mmol/L
- Calcium concentration lower than plasma
- Magnesium concentration above plasma
- Sodium and chloride levels similar to plasma
- Buffer e.g. bicarbonate
- Mannitol
- Additives e.g. procaine, blood
What are the physiological effects of cardioplegia solution on the myocardium?
- High potassium conc. - cardiac arrest in diastole (high extracellular potassium prevents repolarisation)
- Lower calcium level than plasma - maintains integrity of cell membranes
- Lower magnesium level than plasma - stablize cell membrane
- Buffer e.g. bicarbonate to offset metabolic acidosis associated with ischaemia
- Mannitol - reduces tissue oedema, aids clearance of toxic free radicals
- Procaine/blood - reduces arrhthmia at reperfusion and increases oxygen carrying capacity
List two routes by which solutions of cardioplegia can be administered
Anterograde - cannula into ascending aorta/coronary ostia
Retrograde - cannula into coronary sinus
List complications of cardioplegia solution administration
Need at least 6
- Vessel damage from cannulation e.g. dissection or perforation
- Myocardial oedema
- Air emboli in coronaries (bubbles in cardioplegic solution)
- Dislodgement of plaque on cannulation leading to embolic stroke or MI
- Cardioplegic solution unable to perfuse all areas of heart - leaves areas of myocardium warm and active whilst ischaemic
- Fluid overload
- Haemodilution (anaemia and clotting factors)
- Post-operative electrolyte derangement
- Post-operative acid-base disturbance
What dose of herparin is used to achieve full anticoagulation for cardiopulmonary bypass?
300-400 IU/kg
What is the target activated clotting time required prior to cardiopulmonary bypass
And what are the pros and cons of ACT
480s
Pros: rapid response, cheap, familiar
Cons:
State the primary mechanism of action for heparin
Binds to antithrombin II to potentiate inhibition on thrombin and factor Xa
Aside from ACT, list laboratory/POC tests that may be used to determine the effectiveness of heparin anticoagulation in CPB patients, with pros and cons for each
List causes of inadequate anticoagulation after heparin administration for cardiac surgery
Administration errors:
* Wrong drug administered
* Drug not given
* CVC not patent
* CVC not flushed
Increased plasma proteins (therefore reduced free and active drug)
* Acute illness
* Malignancy
* Peri-postpartum
Lack of antithrombin III
* Recent heparin use
* Accelerated consumption due to DIC/sepsis
* Dilution on cardiopulmonary bypass
* Liver cirrhosis - decreased synthesis of antithrombin
* Increased excretion of heparin
* Familial
Give possible adverse reactions to protamine
- Hypotension
- Pulmonary vasoconstriction
- Anaphlaxis
- Unbound protamine inhibits platelet reactivity, adhesion and aggregation so excessive dose can promote bleeding
What is meant by counterpulsation in the context of an intra-aortic balloon pump?
Balloon is inflated in diastole and deflated just before systole
What are the benefits of intra-aortic balloon pump counterpulsation to oxygen delivery to the left ventricle?
- Inflation forces blood proximally, increasing perfusion pressure of the coronary arteries. This increases oxygen delivery to the myocardium
- Deflation decreases afterload, reducing myocardial wall stress and reducing oxygen demand in systole
- Balloon may induce vascular stretch, releasing endothelially derived nitric oxide. This results in coronary artery dilatation and increases blood flow and oxygen delivery
- Potential energy in aortic root during systole is converted to kinetic energy in diastole
State the effect of intra-aortic balloon pump counterpulsation on the output from the left ventricle
- Inflation of the balloon forces blood cephalad and caudad, augmenting the apparent cardiac output from the left ventricle
- Deflation decreases afterload during systole, which also promotes ejection
What are the indications for the insertion of an intraaortic balloon pump?
- Acute heart failure with hypotension
- MI with acute LV failure
- MI with acute mechanical complications causing shock e.g. acute mitral regurgitation
- Low cardiac output after CABG
- Prophylaxis or adjunctive treatment in high risk PCI
- Bridge to definitive treatment in patients with intractable angina
What are the contraindications to insertion of an intraaortic balloon pump?
- Moderate-severe aortic regurgitation
- Aortic dissection
- Aortic aneurysm
- Chronic end stage heart failure with no further treatment options
- Severe untreated peripheral artery disease
Give the anatomical location at which the cephalad end of the balloon of the IABP should be placed
Descending thoracic aorta 2-3cm distal to the origin of left subclavian artery
How is balloon inflation timed when using an IABP
- ECG triggered - inflates with T wave, deflates with peak of R wave
- Arterial pressure waveform triggered - inflates with dicrotic notch (aortic valve closes), deflates just before upstroke of arterial pressure wave form (aortic valve opens)
What are the physiological consequences of mistimed inflation of an IABP
- Early inflation causes increased left ventricular afterload, aortic regurgitation and increased myocardial oxygen demand
- Late inflation causes suboptimal coronary artery perfusion
- Early deflation causes suboptimal reduction in afterload
- Late deflation causes increase in afterload and increase in myocardial oxygen demand
What are the complications of insertion or use of intraaortic balloon pump?
Vascular access/insertion
* Haematoma
* False aneurysm
* Infection
Device use
* Limb ischaemia
* Aortic dissection
* Cardiac tamponade
* Thromboembolism
* Haemolysis
* Balloon rupture and gas embolus
* Requires systemic anticoagulation - bleeding risk
What are the central neurological complications of coronary artery bypass surgery?
- CVA
- Gas embolism
- TIA
- Delerium
- Post-operative cognitive dysfunction
- Ischaemic spinal cord injury
What are the peripheral neurological complications of coronary artery bypass surgery
- Brachial plexus injury (sternal retration pushes clavicles into retroclavicular space)
- Ulnar nerve injury (positioning for radial artery harvesting)
- Phernic nerve injury (IMA harvesting)
- Recurrent laryngeal nerve injury (prolonged intubation with periods of hypotension, or dissection of IMA)
- Saphenous nerve injury (surgical damage when harvesting saphenous vein)
- Intercostal nerve damage (for minimally invasive direct coronary artery bypass where incision is between ribs)
What are the patient risk factors for development of central neurological complications due to coronary artery bypass surgery
- Age
- Hypertension
- Hypercholesterolaemia
- History of stroke
- Diabetes
- Carotid stenosis
- Pre-operative cognitive dysfunction
- History of substance abuse
- Poor LVEF
What are the surgical risk factors for development of central neurological complications after coronary artery bypass surgery
- Duration of surgery
- Microemboli from diseased aorta or CPB circuit
- Rapid rewarming after hypothermia (loss of autoregulation and cerebral oedema)
- Failure to maintain adequate cerebral perfusion pressure during CPB
What are the anaesthetic risk factors for development of central neurological complications after coronary artery bypass surgery
- Low intraoperative MAP, and so CPP
- Prolonged deep hypnotic time
List the intraoperative approaches to minimising the risk of central neruological complications after coronary artery bypass surgery
- Minimally invasive techniques to reduce overall stress response
- Adequate priming of CPB cirtuit and use of bubble traps
- Surgical care to avoid disrupting aortic plaques
- Maintenance of haemodynamic stability to ensure adequate cerebral and cord perfusion pressure
- Careful anticoagulation monitoring and management
- Careful neck positioning
- Monitor and manage acid-base balance
- Optimal blood glucose
- Avoid fast rewarming
What factors can lead to the development of high airway pressures during one-lung ventilation?
- Double lumen tube narrower and more readily obstructed with secretions or blood
- Malpositioned DLT during positioning manouevres
- Excessive tidal volumes
- External compression of breathing circuit
- Atelectasis of ventilated lung
- Bronchospasm
- Inadequate muscle relaxant
- Anaphylaxis
- Pneumothorax
- ALI during prolonged surgery
State the gas used to inflate the balloon of the intra-aortic balloon pump and give a reason why this gas is used
Helium - rapid absorption into blood in the event of balloon rupture, low density so flow will be laminar and the gas is rapidly transferred from the IABP machine to the balloon tip
How does DCM present
- Dyspnoea
- Poor exercise tolerance
- Fatigue
- Arrythmias
- Embolic events
- Sudden death
- Positive result from screening of family members after index case
A 70-year-old male with 50 pack year smoking history with lung cancer presents for pneumonectomy. List other comorbidities this patient may have
- COPD
- IHD
- Pulmonary HTN
- HTN
- Heart failure
- Peripheral vascular disease
- Cerebrovascular disease
- Anaemia
- Poor nutritional status
Give the preoperative physiological measurements used to assess suiability for pneumonectomy
- DLCO, used to predict PPO DLCO
- FEV1, used to predict PPO FEV1
Both give indication of likelihood of post-operative dyspnoea (>60% indicates low risk, <30% consider CPET)
- VO2 peak (measure of cardiopulmonary reserve, pneumonectomy contraindicared at <10mlO2/kg/min)
- Pulmonary artery pressure from ECHO
List contraindications to pneumonectomy
- Non suitability based on physiological testing
- Significant pulmonary hypertension
- Severe valvular heart disease
- Poor ventricular function
- If for cancer: metastatic disease, subdiaphragmatic extension of tumour, nodes in contralateral thorax
What are the indications for pneumonectomy
- Lung tumour (no mets, not below diaphragm, no LN on other side)
- Traumatic lung injury with uncontrolled haemorrhage
- CHronic TB
- Fungal infection- aspergilloma
- Abscess/empyema
- Inflammatory lung disease
- Congenital lung disease
How to optimise a patient for pneumonectomy
- Smoking cessation
- Nutrition
- Prehabilitation physical exercise training
- Management of anaemia
- Optimisation of meds for chronic lung disease
- Optimisation of other co-morbidities e.g. heart disease
Describe how correct placement of a left sided double lumen tube is performed clinically
- Insert DLT under direct vision so that blue cuff is just seen under vocal cords and tube is rotated so that the tip sits in the left bronchus
- Check for B/L chest movement and auscultation of breath sounds when both cuffs are inflated and both lumens are connected to the breathing circuit
- Clamp the tubing to the bronchial lumen, open the bronchoscopy cap - should only have right chest movements + breath sounds
- Unclamp left tubing and replace cap. Clamp tracheal lumen, open tracheal cap - should only have left chest movements + breath sounds
- Confirm with flexible bronchoscopy
List post-operative complications of pneumonectomy
- Atrial tachyarrhythmias
- Pulmonary hypertension, progressive right heart failure
- Bronchopleural fistula
- Nerve damage e.g. phrenic or recurrent laryngeal
- Post-pneumonectomy pulmonary oedema
List the clinical features of cardiac tamponade
- Hypotension
- High JVP/rising CVP
- Muffled heart sounds
- Pulsus paradoxus (exaggerated reduction in systolic pressure during spontaneous ventilation)
- Oliuria
- Increasing vasopressor requirement
- Sudden cessation of drain output
- Tachycardia
- Dyspnoea
- Pericardial rub
- Kussmaul’s sign - JVP does not fall with inspiration
What are the causes of cardiac tamponade
- Acute haemorrhage from:
1. Chest trauma
2. Type A aortic dissection
3. Iatrogenic following cardiology procedures - Pericarditis
1. Infectious
2. Idiopathic
3. Immune
4. Uraemic
5. Malignant
Name the findings in cardiac tamponade
* ECHO
* Chest X-ray
* ECG
* Pulmonary artery catheter
- ECHO: collapse of cardiac chambers, IVC dilatation, leftward shift of intravnetricular septum during spontaneous ventilation, “swinging heart”
- CXR: enlarged or globular cardiac sillhouette, evidence of heart failure e.g. pulmonary oedema
- ECG: sinus tachycardia, atrial arrythmias, low voltage QRS complexes, electrical alternans
- Pulmonary artery catheter: equalisation of diastolic pressures in all heart chambers, raised pulmonary wedge pressure
What is the surface landmark for needle insertion for pericardiocentesis
- Fifth left intercostal space close to sternal margin
List the complications of pericardiocentesis
- Laceration of ventricle
- Puncture of abdominal viscera
- Pneumopericardium
- Arrythmias
- Pericardial decompression syndrome
- Pneumothorax
What are the haemodynamic goals whilst assessing a patient with tamponade
- Maintain preload, replace lost volume
- Maintain sinus rhythm
- Avoid bradycardia
- Maintain systemic ascular resistance to maintain coronary perfusion
- Maintain cardiac contractility (avoid myocardial depressants)
In reality - call for help (Senior, cardiothoracics)
“Fast, full and tight”
What are the immediate effects on the left ventricle of initiating positive pressure ventilaton during tamponade
- Acute rise in intrathoracic pressure compresses pulmonary vasculature
- Leads to acute rise in venous return to left ventricle
- Shifts interventicular septum towards the right and temporarily increases stroke volume
- However, the rise in intrathoracic pressure causes reduction in venous return to right heart, reduced preload to left ventricle and then further reduction in cardiac output
List the classical symptoms of aortic stenosis
Angina
Dyspnoea
Syncope
Give the following echocardiographic values for severe AS:
* Peak aortic flow volocity
* Mean transaortic pressure gradient
* Valve area
- Peak aortic flow volocity: 4m/s
- Mean transaortic pressure gradient: 40mmHg
- Valve area: 1cm2
Which factors would favour TAVI over surgical aortic valve replacement?
Patient factors
* Increased age
* Severe co-morbidities
Surgical factors
* Previous cardiac surgery
* Previous aortic valve replacement (otherwise would require redo sternotomy)
* Favourable vascular access
* Heavily calcified aorta
* Only aortic valve surgery required
* Chest wall deformity
What is the absolute contraindication to TAVI?
Infective endocarditis
Relative: aberrant anatomy, no benefit to QoL or life expectancy
What are the options for anaesthesia in a patient presenting for TAVI?
- Local anaesthesia
- Local anaesthesia with conscious sedation
- General anaesthesia
What are the haemodynamic goals when anaesthetising a patient undergoing TAVI?
- Maintain preload - ensure ventricular filling
- Maintain sinus rhythm - ventricular filling is dependent on atrial contraction (due to LVH)
- Maintain normal heart rate - bradycardia in fixed output state, tachycardia affects diastolic perfusion time
- Maintain contractility
- Maintain afterload - to maintain coronary perfusion (CPP=DBP-LVEDP)
What are the causes of haemodynamic instability in a patient undergoing TAVI?
- Major haemorrhage due to injury or aortic root or intrathoracic blood vessels
- Arrhythmia
- Cardia ischaemia (occlusion on ostia by implant)
- Deliberate - rapid ventricular pacing to 200bpm performed whilst valve deployed to prevent its migration
Haemodynamic goals for valve lesions
Give causes for hypoxaemia in one lung ventilation
Patient factors
* Chronic lung disease
* Obesity
* Increased age
Anaesthetic factors
* Use of vasodilators (reduced hypoxic pulmonary vasoconstriction)
* High dose-volatile anaesthesia
* Inadequate pre-oxygenation prior to OLV
Surgical factors
* Previous pulmonary resection of dependent lung
* OLV in supine position
* Alternating OLV
Risk factors for post-operative pacemaker dependence
CPB
Long CPB time
More than one valve
Reoperation
Older age
Pulmonary HTN
Renal failure
Diabetes
Pre-operative arrythmia
What is the risk with asynchronous pacing?
R-on-T phenomenon leading to VF or polymorphic VT
Left coronary perfusion pressure
= Aortic diastolic pressure-left ventricular end diastolic pressure
Explain the diagram
- Unassisted aortic end diastolic pressure
- Systolic pressure, unaugmented
- Diastolic pressure augmented by balloon pump
- Reduced aortic end diastolic pressure
What are the criteria for lung transplant
- Chronic end stage lung disease with >50% risk of death in 2 years
- With transplant, likely to survive >5 years
Give three contraindications to lung transplant
- Recent malignancy
- Significant dysfunction in another organ
- Alcohol or drug abuse
- BMI>35
Pre-operative tests for lung transplant
- Bloods: FBC, U&Es, LFTs, CRP
- TTE to assess cardiac function, RV pressure and PH
- CT chest to rule out occult malignancy, assess potency of great vessels
- Right heart catheter to evaluate pulmonary hypertension
- Pulmonary function tests to evaluate pre-operative lung function and suitabiliity for transplant
Give two reasons for “on-pump” lung transplant
- Severe pulmonary hypertension
- Patient already on ECMO
Aetiology, pathophysiology and clinical features of dilated cardiomyopathy
- Aetiology: idiopathic, familial, alcohol, post-viral,
- Pathophysiology: progressive dilatation of ventricle(s) leads to impaired systolic function
- Clinical features: right heart failure e.g. fatigue, peripheral oedema, acites, dyspnoea, arrhythmia, death
Aetiology, pathophysiology and clinical features of restrictive cardiomyopathy
- Aetiology: idiopathic, amyloidosis, sarcoidosis
- Pathophysiology: fibrotic changes to myocardium and subendocardium reduce compliance and end diastolic pressure increases
- Clinical features: fatigue, orthopnoea, dyspnoea, oedema
Aetiology, pathophysiology and clinical features of hypertrophic cardiomyopathy
- Aetiology: autosomal dominant
- Pathophysiology: hypertrophy of ventricular cells leads to diastolic dysfunction
- Clinical features: angina, non-sustained VT, sudden death
After what ischaemic time is there increased risk of graft dysfunction in lung transplant?
5.5hrs
Which disease group is most likely to develop primary graft dysfunction after lung transplant?
Pulmonary hypertension
What are the signs of primary graft dysfunction after lung transplant
- Impaired oxygenation
- Diffuse opacities on chest XR
What are the advantages of blood cardioplegic solution
- Assists oxygen delivery
- Free radical scavenging
- Less myocardial oedema
- Delivery of other nutrients
Define cardiomyopathy
- Myocardial disorder where function and structure of heart muscle is abnormal
- Which cannot be attributed to IHD, HTN, valvular or congenital heart disease
Give the haemodynamic goals for the cardiomyopathies, AS and MR
DCM - avoid TACHYCARDIA not bradycardia (coronary perfusion during diastole)
Causes of impaired hypoxic pulmonary vasoconstriction during OLV
Increased pulmonary artery pressure:
* Use of vasopressors
* Asthmatic patient with intrinsic PEEP to non dependent lung
* Atelectasis of dependent lung
Other:
* Use of vasodilators
* Failure of lung collapse
* Turning to supine position
Physiological implications of a transplanted heart
- Resting HR 90bpm
- Baroreceptor reflex lost - no tachycardia in response to hypotension
- No tachycardia to light anaesthesia or laryngoscopy
- Pneumoperitoneum does not cause reflex bradycardia
- Dysrhymias more common
- Cardiac output dependent on preload
Pharmacological implications of a transplanted heart
- No reponse to vagolytics e.g. glycopyrrolate and atropine
- No response to indirect sympathomimetics
- Exaggerated response to adrenaline and noradrenaline
- Exaggerated response to adenosine, use smaller doses
- Digoxin does not correct AF
Anaesthetic considerations in a patient with transplanted heart
- Preserve graft: maintain coronary perfusion pressure perioperatively
- Mitigate increased risks: awake art line, external pacing available, normovolaemia
- Immunosuppression: scrupulous aseptic technique with lines, continue immunosuppression perioperatively
MOA of enoximone and milrinone
- PDEI 3
- Increases intracellular cAMP
- Increased calcium influx during phase 3 cardiac action potential to increase force of contraction
- Increased intracellular cAMP in smooth muscle causes vaso-relaxation
