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James' final FRCA SOE > Cardiac > Flashcards

Cardiac Flashcards

1
Q

You pick up a murmur prior to an elective inguinal hernia repair - do you proceed without an echo?

A

Murmur MAY be a sign of cardiac disease, but could be physiological in nature.

If they have NO SYMPTOMS, good functional status and a normal ECG then do not need echo prior to minor or intermediate surgery.

If symptomatic +- abnormal ECG OR undergoing major surgery then worth delaying for further Ix. including echo

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2
Q

What is the pathophysiology of aortic stenosis?

A

Progressive obstruction of aortic valve commonly caused by senile calcification of normal valve, congenital bicuspid valve or rheumatic heart disease

  1. Increasing LVOT obstruction causes:
    - LVH
    - Reduced compliance (diastolic dysfunction)
    - Myocardial supply/demand mismatch
  2. Ventricle dilatation with disease progression
    - Subendocardial ischaemia
    - Reduced LVEF
    - Pulmonary congestion

Symptoms to ask about
1. Angina
2. Dyspnoea
3. Syncope/pre-syncope

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3
Q

Severity grading for AS on echo doppler studies

A

Valve area
Normal = 3-4cm2
Mild = 1.5-2.9cm2
Moderate = 1-1.4cm2
Severe = <1.0cm2

LV-aortic gradient
Normal = <5mmHg
Mild = 5-25mmHg
Moderate = 25-40mmHg
Severe = >40mmHg

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4
Q

Other cardiac ix. for AS in addition to valve area/gradient ?

A

LV size
LVEF and fractional shortening
Aorta, MV, LA, PA pressure, RV function, LVOTO presence

ECG
- Conduction abnormalities
- LV hypertrophy/strain
- Ischaemia

Angiography ?CAD

CT/MRI of aortic root

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5
Q

Indications for surgical AVR for AS

A

High risk procedure. Undertaken by MDT.
Indications include:
- Severe AS with symptoms
- Asymptomatic severe AS, with EF <50%
- Asymptomatic severe AS with risk rapid progression, or presenting for major surgery
- Moderate AS in context of other cardiac procedure e.g. CABG

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6
Q

Talk about factors favouring surgical AVR vs. TAVI

A

Surgical AVR with sternotomy
Patient factors:
- EuroSCORE <10% (fitter patient cohort)
Surgical factors:
- Short distance between coronary ostia and valve annulus
- V.small valve areas
- Necessity for additional procedures e.g. CABG

TAVI
Patient factors:
- Comorbidity, frailty, higher euroscore

Surgical factors:
- Amenable valve
- Previous cardiac surgery with inc. risk

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7
Q

Complications of valve deployment at TAVI

A

Paravalvular leak
Cardiac arrest - vent. asystole/VF/PEA
AV nodal block
Coronary ostia obstruction
Device embolisation into aorta
Rupture of aortic annulus
Stroke due to embolus of calcified native valve

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8
Q

Aortic regurgitation causes

A

Primary - rheumatic heart disease, endocarditis
Secondary - dilated aortic root
- Marfan’s
- Dissection
- Ank spong

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9
Q

Aortic regurgitation severity

A

Doppler studies
Jet width into aortic cavity (as %LVOT diameter)
Mild <25%
Severe >60%
Pressure half time (time req. for peak pressure to dec. by half)
Mild >500ms
Severe <250ms

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10
Q

Aortic regurgitation indications for surgery

A

Severe symptomatic aortic regurgitation
Severe asymptomatic aortic regurgitation but LVEF <50%
Significant enlargement of ascending aorta

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11
Q

Mitral stenosis severity grading

A

Mitral valve area
- Normal 4-6cm2
- Symptomatic <1.6-2.5cm2
- Severe <1.0cm2

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12
Q

Other considerations with mitral stenosis

A

Commonly in AF
May cause pulmonary HTN and RV failure
Measure ventricular function

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13
Q

Severity of mitral regurgitation

A

Regurgitant jet area
- Mild <4cm2 (or <20% of LA)
- Severe >8cm2 (or >40% of LA)

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14
Q

What is pulsus paradoxus?

A

Defined as drop in systolic BP of >10mmHg during the inspiratory phase

May occur in
- Cardiac tamponade
- COnditions where the RV is distended: acute severe asthma or COPD exacerbations

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15
Q

Physiology of pulsus paradoxus ?

A

Normally you expect a decrease in systolic BP during inspiration because:
Negative pressure increases blood flow from vena cavae to RA
Blood pools in lungs and decreases pulmonary venous return to LA
The relative inc. in RA pressure with dec. LA preload results in drop in systolic BP

This is exagerrated in situations where
- Venous return and ventricular filling is impaired e.g. tamponade
- High pulmonary afterload e.g. asthma
- High negative intrathoracic pressure e.g. asthma/copd

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16
Q

4 main issues following cardiac surgery

A
  1. Arrythmias
  2. Bleeding
  3. Tamponade
  4. Pulmonary HTN
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17
Q

What 5 components does a CPB circuit allow manipulation of

A
  1. Gas exchange
    - Membrane oxygenator
    - Occurs via concentration gradients
    - Increasing FiO2 increases oxygenation
    - Increasing gas flow removes CO2
  2. MAP
    - Non pulsatile, set by flow rate
    - SVR altered pharmacologically
  3. Temperature
    - Heat exchanger (conduction)
  4. Haematocrit
    - Add volume to reservoir
    - Remove volume by ultrafiltration
  5. Acid-base strategy
    - pH stat
    - Alpha stat
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18
Q

Complications of CPB

A

Intraoperative
- Consumptive coagulopathy
- Haemolysis and platelet damage
- Aortic dissection
- Gas embolisation from heart not ‘de-aired’

Post-operative
- Neurological damage
- a) Perfusion related
- b) Embolic
- i) surgical - valve surgery
- ii) patient - aortic atheroma, diabetes, prior stroke, age

  • SIRS response

MINIMISED BY - normothermia, normoglycaemia, adequate perfusion pressure, confirmation of de-airing

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19
Q

Anaesthetic role during CPB

A

Anticoagulation
- 300u/kg heparin given via CVC
- ACT >400s pre-bypass and every 30 minutes thereafter
- Reversal with protamine when requested - given slowly and peripherally to minimise systemic hypotension/pulmonary hypertension

Temperature control
- Allow to fall or actively lower during CPB
- Bring up to normothermia prior to off CPB

Anaesthesia maintanence
- Infusion or volatile via CPB circuit

Acid-base/electrolytes
- Normalise prior to coming off bypass

Arythmia
- Control with medication or DC cardioversion

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20
Q

Purpose of cardioplegia solution

A
  1. Induce asystole therefore provide motionless surgical field
  2. Provide a degree of myocardial protection
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21
Q

Tell me about cardioplegia solutions

A

Generally contain mixture of potassium, magnesium, procaine, bicarb nicorandil, apartate,

Cold crystalloid
Cold blood
Warm blood

Blood has theoretical advantage of inc. O2 delivery, reduced oedema, inc. buffering

High K+ conc (20mmol/L) reduces myocardium membrane potential -90 to -50 which prevents repolarisation and inactivates fast Na+ channels and therefore upstroke

Induces diastolic arrest

Can be given anterograde or retrograde
Retrograde if significant coronary disease

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22
Q

Any non-cardioplegia techniques?

A

Off pump
VF induced - should not exceed >10mins

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23
Q

Tell me about advantages of temperature effects on CPB?

A

Advantages
- Dec. myocardial o2 consumption and total body o2 consumption

Disadvantages
- Coagulopathy, impaired myocardial cell memb function

24
Q

What temperature targets are there during CPB

A
  1. Normothemic
  2. Hypothermic - 25-32 deg generally
  3. Deep hypothermic circulatory arrest
    - Cerebral protection with optimal conditions
    - 15-18deg
    - Complex procedures involving arch
    - Up to 30mins at 18deg allows neuroprotection

Longer procedures need selective anterograde cerebral perfusion

25
Tell me about causes of RV failure
1. Intrinsic RV failure - Infarction - Cardiomyopathy 2. Increased RV afterload - Pulmonary hypertension (many causes) e.g. left heart disease, intrinsic lung disease - PE (acute vs. chronic) 3. RV volume overload - LV failure - Left-to-right shunt (ASD or VSD)
26
Signs of right heart failure
Peripheral oedema Ascites Raised JVP (should be <4cm height above sternal angle) Tender hepatomegaly Pansystolic tricuspic regurg murmur Loud P2 raised PA pressure 3rd heart sound
27
Echo signs of RV failure
Increased RV:LV ratio Loss of crescent shape of RV Flattening of interventricular septum Tricuspid regurgitation
28
Management of right heart failure
1. Treat underlying cause e.g. PCI for MI, thrombolysis/clot retrieval for PE 2. Reduce PVR - Correct acidosis - PaO2 / PaCO2 optimise - Pulmonary vasodilaters e.g. inhaled nitric, sildenafil, prostacyclin 3. Restore right coronary perfusion pressure - MAP >65 4. Improve contractility - Inotropes 5. Reduce RV pre-load with diuretics 6. Mechanical support - RVAD, ecmo
29
6 core symptoms of cardiac disease
ANGINA DYSPNOEA ORTHOPNOEA / PND SYNCOPE PALPITATIONS EXERCISE LIMITATION
30
How can you stratify angina?
Canadian Cardiovascular Society Class I = angina with strenuous exercise Class II = angina causing slight limitation (e.g. >1 flight of stairs) Class III = angina causing marked limitation (e.g. 1 flight of stairs) Class IV = angina with ANY physical activity or rest
31
Tell me about ways to quantify functional capacity in history?
New York Heart Association classification of functional capacity I = no limitation of activity II = slight limitation in physical activity III = marked limitation in physical activity but comfortable at rest IV = discomfort at rest Combined with American Heart Association AHA objective assessment A = no evidence B = objective evidence of minimal disease C = objective evidence of moderate disease D = objective evidence of severe disease Duke Activity Status Index questionnaire 12 questions related to ability to perform tasks and exercise Relates to METs metabolic equivalent of tasks <4 METS = high risk of adverse outcomes
32
Tell me about risk scoring systems for cardiac surgery and what they encompass
EuroSCORE Patient related e.g. age, sex, CKD, prev. cardiac sx. , critical pre-op state Cardiac related e.g. unstable angina, LV dsyfunction, pulmonary HTN, recent MI Operation related e.g. emergency sx, thoracic aorta, operation other than isolated CABG Parsonett Patient related Cardiac related Surgery related
33
Tell me about a risk scoring system for cardiac events in NON-CARDIAC surgery
Revised Cardiac Risk Index (6 things) - High risk surgery - Pre-op IHD - Pre-op CCF - Pre-op CVA - Pre-op elevated creatinine - Pre-op insulin use
34
What is congenital heart disease?
Congenital heart disease refers to a STRUCTURAL abnormality of the heart which is present at brith and has potential functional significance. Excludes by convention cardiomyopathies and congenital arrythmias Spectrum of severity 90% of children with Cong HD survive to adulthood Prevalence is increasing
35
How can adult congenital heart disease be classified
Adults have often had interventions therefore better classified according to complexity Compare with children who are classified according to structural features
36
Examples of simple lesions adult congenital heart disease
Simple lesions - Repaired e.g. VSF - Unrepaired e.g. small ASD, isolated valve disease May require cardiology follow up Often can have surgery in non-specialist centres
37
Examples of moderate complexity lesions adult congenital heart disease
Unrepaired: VSD with associated anomaly e.g. valve disease Moderate to severe pulmonary stenosis Unrepaired ductus arteriosus Repaired Tetralogy of fallot Patients require cardiology follow up, ongoing risk of complications and reduced life expectancy Should be discussed with specialist centres
38
Examples of severe complexity lesions adult congenital heart disease
Adult cyanotic heart disease Single-ventricle pathology Corrected Transposition of Great Arteries (TGA) Eisenmenger's syndrome Double-outlet ventricle High risk of significant complications High risk of perioperative deterioration, surgery performed in specialist centres
39
Specific factors for consideration in adult congenital heart disease
Associated non-cardiac disease Psychological factors Arrythmias and potential effect of arrythmias Potential effect of negatively inotropic / vasodilatory effects of anaesthetic agents Potential effect of ventilation strategies Thromboprophylaxis and antibiotic prophylaxis
40
Why might women with adult congenital heart disease tolerate pregnancy poorly?
During pregnancy - Increase in total blood volume, increase in cardiac output, increase HR and peripheral vasodilation During labour - Further increase in blood volume (autotransfusion), increased cardiac output, sympathetic surge
41
General principles for women with adult congenital heart disease and labour
Discussion with specialist centre, likely will need referral Most likely approach for severe congenital cardiac disease will be - Combines spinal-epidural with cautious doses to avoid sudden haemodynamic changes - If high risk of deterioration consider general anaesthesia in cardiac theatres with bypass/ ecmo available If attempting normal labour - Early epidural to mitigate sympathetic response Anticoagulation must be considered
42
What dose CHA2DS2VASc stand for
C = CHD (score 1) H = Hypertension (score 1) A = Age >75 (score 2) D = Diabetes (score 1) S = Stroke/TIA (score 2) V = Vascular disease or MI (score 1) A = Age 65-74 (score 1) Sc = Sex category female (score 1) Max score 9 Consider oral anticoagulants Males 1 Females 2
43
How can I.E be diagnosed
Duke's criteria 2 major 1 major and 3 minor 5 minor Major - 2x seperate BCs taken at different sites - CT/echo evidence of endocarditis e.g. vegetation Minor Risk factor Temp >38 Embolic phenomena e.g. janeway lesions, ischaemic limb Immunological phenomena e.g. roth spots, osler nodes, +ve RF Micro evidence that doesn't meet major criteria e.g. 1x positive sample
44
Risk factors for I.E
Cardiac vs. non-cardiac Cardiac - Valve prosthesis - Bicuspid AV - MV prolapse - Rheumatic heart disease - Indwelling cardiac devices Non-cardiac - Immunocompromised e.g. malignancy, DMARDs, steroids, diabetic - Indwelling lines e.g. dialysis line - IV drug use
45
Common causative organisms for I.E
Common - these are often culture +ve Streptococci (viridans, bovis) Staphylococcus (aureus + coag -ve staph) Enterococci Less common - HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella Fungi: Candida, Aspergillus
46
Indications for surgery with I.E
Embolic event with large intracardiac vegetations (>10mm) Severe valvular dysfunction with large vegetation (>10mm) Very large vegetations which may obstruct outflow (>15mm) Aortic root abscess
47
How does I.E differ in IV drug users
Usually effects Right side of the heart causing 1. Pneumonia and empyema 2. Septic PE Causative organisms: Pseudomonas aeruginosa Staphylococcus aureus Fungal species
48
Anaesthetic pre-assessment history in a patient with a cardiac transplant
In addition to my usual anaesthetic pre-operative assessment I would focus on the following: 1. Aetiology of cardiac failure and date of transplant - Any systemic co-morbidities e.g. vasculopathy with atherosclerosis in ischaemic cardiomyopathy - Congenital abnormalities 2. Functional assessment - Indication of graft function and heart failure 3. Chest pain/angina - Evidence of allograft vasculopathy 4. Presence of pacemaker, when inserted, why 5. Current medication including immunosupressant and heart failure medication 6. Screen for evidence of active infection
49
Anaesthetic pre-assessment pertinent investigations in cardiac transplant
Echocardiography - graft function ECG Exercise tolerance Coronary angiography - allograft vasculopathy Endomyocardial biopsy - graft rejection Bloods: Renal dysfunction Liver dysfunction Bone marrow suppression CXR
50
What atypical organisms are associated with immunosuppresion?
1. CMV - Re-activation of previous or primary CMV - Can effect LUNGS, GIT, retina - CMV-negative blood to be used in transfusion 2. Toxoplasma - Encephalitis, myocarditis, pneumonitis 3. PJP 4. Legionella 5. Candida albicans 6. HSV
51
Physiological changes post cardiac transplant
Suture line from donor atria to recipient atria with no autonomic inervation to donor heart Resting HR maintained by donor SA node activity HR 90-100 Normal reflex changes with peritoneal stretching/laryngoscopy/awareness are lost No compensatory tachycardia in response to hypotension - Hypovolaemia poorly tolerated Exercise results in blunted increase in heart rate as entirely dependant on adrenal catecholamine release MI is 'silent' - no pain
52
Pharmacology considerations post transplant
Vagolytic drugs useless e.g. atropine/glyco INDIRECTLY acting sympathomimetics e.g. ephedrine have limited effects GTN no reflex tachy Digoxin retains +ve inotropy but no HR effects Sux and neostigmine have no bradycardic effects Autonomic denervation means upregulation of donor receptors Adenosine effects x4 Adrenaline use smaller doses
53
Anaesthetic "how to" for cardiac transplant
Peri-operative Senior support, cardiac centre ideally Careful positioning - fragile skin, steroids Monitoring - AAGBI, CO monitoring, CM5 if ischaemia risk Lines - 16G, CVC, art line Trained assistant Resus drugs all drawn up including vasopressor/inotrope infusions External pacemaker device available Steroid replacement with hydrocortisone and consider infusion Prohylactic antibiotics Induction - smooth, titrated, haemodynamically stable with art line placed before Airway oral over nasal (sinusitis risk), careful as gingival hypertrophy bleeding gums Maintanence - volatile low MAC, entropy monitoring Emergence - extubate vs. keep intubated, assess Post op Analgesia/disposition Likely HDU/ITU Lines kept in as brief as possible Caution NSAIDS Input with other teams re: restart immunosuppresants
54
Cardiac transplant obstetric patient increased risk of what
Pre-eclampsia Eclampsia Premature delivery Gestational diabetes Allograft rejection
55
What findings can be diagnosed with a doppler ECHO in a patient with valvular heart disease?
Chambers - size, function, wall motion abnormalities, thrombus presence Septum - thickening/thinning, motion abnormalities Valves - structural anatomy, thickening, cusp number, calcification, stenosis/regurg Measurements: - Chamber pressures - Aorta and pulmonary vasculature - Peak velocity across valves - Mean gradients - Ejection fraction
56
What are the cardiac conditions where pregnancy is ABSOLUTELY contraindicated?
WHO CLASS IV stratification: Pregnancy contraindicated, termination should be discussed - Pulmonary hypertension of any cause - Severe systemic ventricular dysfunction (LVEF <30%, NYHA class III-IV) - Severe symptomatic MS and AS - Marfan's syndrome with aortic root dilation >45mm - Native severe COA
57
What are the cardiac conditions where pregnancy is RELATIVELY contraindicated?
Severe aortic and mitral stenosis Marfan's syndrome with significant aortic root dilatation Prosthetic valves requiring anticoagulation Cyanotic heart diseases

James' final FRCA SOE (16 decks)

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