CARDIO Flashcards

(389 cards)

1
Q

What is cardiomyopathy?

A

Myocardial disorder whereby the heart muscle is structurally and functionally abnormal.
That cannot be explained by coronary artery disease, HTN, valvular disease or congenital heart disease

They may be genetic or acquired

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2
Q

What are the different types of cardiomyopathy?

A
  • Dilated cardiomyopathy – systolic dysfunction
  • Restrictive cardiomyopathy – impaired ventricular filling
  • Hypertrophic obstructive cardiomyopathy – diastolic dysfunction
  • Arrhythmogenic RV cardiomyopathy
  • Unclassified
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3
Q

What are the causes of dilated cardiomyopathy?

A
  • Often idiopathic
  • Familial (e.g., genetic causes such as Duchenne’s and Becker muscular dystrophy)
  • Post viral myocarditis
  • Drugs (e.g., chemotherapy, alcohol)
  • Pregnancy
  • Nutritional deficiencies
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4
Q

What is the pathophysiology of dilated cardiomyopathy?

A
  • LEFT ventricular dilation
  • As LV enlarges, the ability for actin / myosin to overlap and contract reduces and thus ejection fraction reduces – systolic dysfunction
  • Progresses to HF
  • Other complications
    o Thrombus formation and embolic disease
    o valvular disease due to progressive enlargement of ventricles
    o Increased volume - increases diastolic pressures, impedes coronary blood flow
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5
Q

What are the clinical features of dilated cardiomyopathy?

A
  • Signs and symptoms of heart failure (SoB, poor exercise tolerance, fatigue, ascites, peripheral oedema)
  • Arrhythmias
  • Embolic events
  • Sudden death
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6
Q

How is dilated cardiomyopathy managed?

A
  • Medical management of heart failure (Beta blockers, Diuretics, ACE inhibitors/ARBs, Anticoagulants, SGLT2 inhibitors)
  • Cardiac devices (Cardiac resynchronisation pacing therapy, Implantable cardiac defibrillator, LV assist device)
  • Surgical (Partial left ventriculectomy, may require heart transplant)
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7
Q

What are two predictors of poor outcome in patients with dilated cardiomyopathy?

A
  • LVEF <20%
  • Elevated left ventricular end diastolic pressure
  • LV hypokinesia
  • Non-sustained VT
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8
Q

How would you anaesthetise someone with dilated cardiomyopathy?

A
  • If possible, regional and avoid GA for haemodynamic stability
  • Awake arterial line
  • Avoid excessive anaesthetic agents and myocardial depressants - Slow IV induction, Opioids to reduce propofol, Use BIS
  • Haemodynamic goals met
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9
Q

What are the haemodynamic goals in anaesthetic for someone with dilated cardiomyopathy?

A
  • Maintain sinus rhythm
  • Adequate volume loading/preload
  • Maintain normal SVR- Prevent increases in afterload and sudden hypotension
  • Avoid myocardial depression
  • avoid tachycardia - increases O2 demand, reduces filling time of heart and coronary
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10
Q

What monitoring techniques can help guide the anaesthetic in those with dilated cardiomyopathy?

A
  • Transoesophageal ECHO – dynamic assessment of heart filling and cardiac output
  • Oesophageal doppler – SV assessment
  • Invasive arterial blood pressure monitoring – stoke volume variation, acid base balance via frequent blood sampling , beat to beat blood pressure to have tighter control
  • Depth of anaesthesia monitoring to reduce amount given
  • Cerebral oxygenation monitoring – reduce risk of post op cognitive dysfunction
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11
Q

What is the aetiology of hypertrophic cardiomyopathy?

A

Autosomal dominant inheritance

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12
Q

What is the pathophysiology of hypertrophic cardiomyopathy?

A
  • Hypertrophy of LV and results in LV outflow obstruction
  • Diastolic impairment first as hypertrophy develop
  • (systolic impairment is a late sing)
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13
Q

What are the ECHO findings in hypertrophic obstructive cardiomyopathy?

A
  • Septal hypertrophy
  • Dynamic LVOT obstruction = Systolic anterior motion of mitral valve and increased aortic pressure gradient
  • LV hypertrophy and small cavity
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14
Q

how are pts with HOCM anaesthetised?

A

same as aortic stenosis

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15
Q

What is the pathophysiology of restrictive cardiomyopathy?

A

Stiff ventricles impair diastolic filling, causing diastolic dysfunction and heart failure.

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16
Q

Describe the anaesthetic goals of restrictive cardiomyopathy

A
  • Very dangerous as the ionotropic effects of anaesthetic agents can be catastrophic
  • Consider ketamine and aim for spontaneous ventilation
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17
Q

What is arrhythmogenic RV cardiomyopathy?

A
  • Complex genetic and environmental interplay triggers myocardial cells in RV to be replaced by fibrofatty tissue
  • These abnormal myocardial cells may form re-entry electrical circuits with bundle branch block and subsequent arrhythmias
  • Progresses to regional wall motion abnormalities and right heart failure
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18
Q

What are the management options for arrhythmogenic RV cardiomyopathy?

A
  • ICD
  • Heart transplant
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19
Q

What is aortic stenosis?

A

Progressive obstruction of the aortic valve leading to LV outflow obstruction.

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20
Q

What are the causes of aortic stenosis?

A
  • Degenerative calcification with age – starts with sclerosis
  • Bicuspid valves – promote turbulent flow and calcification at a younger age
  • Rheumatic fever
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21
Q

What are the pathological changes seen with worsening aortic stenosis?

A
  • Narrowing of aortic valve
    o LV outflow obstruction
    o Bernoulli principle – lower diastolic aortic pressure – reduced coronary perfusion
  • LV hypertrophy to compensate
    o Increased O2 demand
    o Diastolic dysfunction – impaired filling and relaxation – limits SV and CO
    o Increased LV EDP – reduced myocardial perfusion and O2 supply
    o Overall supply / demand mismatch – risk of ischaemia
  • LV failure lead to pulmonary congestion
  • Eventually LV dilation
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22
Q

What causes ejection fraction to deteriorate with aortic stenosis over time?

A
  • Increased narrowing of valve area
  • Increased hypertrophy and reduced filling
  • Myocardial dysfunction from ischaemia
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23
Q

What are the symptoms for aortic stenosis?

A
  • Angina
  • Heart failure/dyspnoea
  • Syncope
  • sudden death
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24
Q

Assessment of Aortic stenosis

A
  • Hx and examination
  • Severity assessment ..
    o ECHO – valve area, EF, peak velocity, pressure gradient, other abnormalities e.g. valves
    o Left heart catheterisation and pressure measurements
    o CT / MRI heart
    o CPET
    o Low dose dobutamine stress test + ECHO / left heart catheter
  • Associated complications
    o ECG, BNP
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25
What is the grading for aortic stenosis ?
26
What are the methods for treating aortic stenosis?
- Open surgical repair – gold standard - Transcatheter aortic valve implant – TAVI - Balloon valvuloplasty – no long term benefits, bridging / palliative therapy
27
What are the complications of aortic stenosis repair?
- Open surgical repair o Bleeding o Arrhythmias – AF o Stroke o Mediastinitis / infection - TAVI o Bleeding – retroperitoneal, intrathoracic vessels o Arrhythmias – injury to conduction system – AV block o Stroke – embolus of atheroma / calcified valve o Infection o Aortic annulus rupture or paravalvular regurgitation
28
When is open aortic valve surgical repair indicated over TAVI?
- Clinically indicated e.g. severe AS + symptoms / EF < 50% - (for TAVI or open) - If young and fit enough – better long term outcomes - TAVI contraindicated e.g. I.E , valve anatomy - Having other cardiac surgery anyway e.g. CABG - Need for mechanical valve
29
When is TAVI contraindicated?
* Absolute: Infective endocarditis * Relative: Small annulus / difficult anatomy, severe co-morbidities and unlikely to improve QoL
30
When is TAVI indicated over open repair of aortic valve
- Frail / comorbid e.g. age >75 - Previous CABG / sternotomy - Chest wall deformity
31
Compare TAVI and open repair
- Open – o Gold standard , preferred for younger fitter patients o longer hospital stay o Most complications are higher with open repair o Can implant mechanical or bioprosthetic valves - TAVI o Can only use bioprosthetic valves o Less invasive – preferred in elderly o Less complications however less definitive
32
What are the types of valves that can be used in aortic stenosis repair?
- Mechanical o Life long coagulation, more durable , better for younger patients - Bioprosthetic o Made from animal tissue, no need for long term anti coag, lasts 10-15 yrs – better for elderly
33
What is balloon valvuloplasty?
Balloon placed across aortic valve and then inflated to decrease valvular pressure gradient.
34
What are the routes available for a TAVI?
* Femoral artery - commonest * Also subclavian / carotid * Transaortic – mini sternotomy / thoracotomy * Transapical – via thoracotomy
35
Describe the surgical process of a TAVI
- A stiff guidewire is advanced from the femoral artery to the aortic valve using fluoroscopic guidance - A brief period of systemic hypotension is achieved by rapid pacing – 180 to 220bpm. During this time the native valve is dilated by balloon aortic valvuloplasty - The TAVI is then positioned.
36
How would you anaesthetise someone for a TAVI?
- Option – local , local + sedation, GA o GA for uncooperative patient or non femoral approach - Full AABGI monitoring - Heparin given 3000-5000 units ACT >250 s - Haemodynamic goals o Maintain SVR, preload, contractility, Sinus rhythm, tight HR control
37
What are the haemodynamic goals when anaesthetising someone with aortic stenosis?
- **Maintain Sinus rhythm** – CO more dependant on atrial contraction (40%) o Electrolytes , acid base, hypoxia/ hypercapnoea, antiarrhythmics - **Maintain SVR** – MAP dependant on SVR now CO reduced – ensures coronary perfusion o Vasopressors , avoid spinal - **Tight HR control** o Bradycardia – reduced CO o Tachycardia – reduces filling time / coronary perfusion and increases O2 demand = Good analgesia / opioids on laryngoscopy - **Maintain preload** o Optimises CO , ensures max filling of impaired LV - **Maintain contractility** o Supports LV in pumping against outflow obstruction o **Minimise cardiac depressants, ionotropes** * Maintain sinus rhythm * Maintain SVR * Tight HR control * Maintain preload * Maintain contractility
38
What are the causes of haemodynamic instability in those having a TAVI?
- Bleeding o Aortic injury / femoral injury o Aortic dissection o Tamponade - Arrhythmias – AVN block - Rapid ventricular pacing during valve deployment – reduces CO - Aortic regurgitation - Ischaemia – blockage of coronary ostium - Other general o Pain / anxiety – HTN / tachy o Fasting – dehydration o Anaesthetic – drop SVR / myocardial depressant
39
Do all patients with a murmur require an ECHO before surgery?
- No if good functional capacity and minor op then not required - If symptomatic or major op or ECG changes – then required
40
What are the causes of aortic regurgitation?
* Rheumatic heart disease * Endocarditis * Autoimmune diseases (e.g., SLA, RA) * Dilated aortic root acute - aortic dissection
41
How is aortic regurgitation assessed?
- Hx , examination - ECHO – regurgitation fraction / jet, LV ejection fraction, LV end diastolic / systolic volume
42
What are the indications for surgery in aortic regurgitation?
* Severe symptomatic AR * Severe asymptomatic with LVEF <50% * Significant enlargement of ascending aorta
43
How is aortic regurgitation managed?
- Conservatively / surgical - if it develops acutely e.g dissection it is an emergency
44
What are the causes of mitral stenosis?
Rheumatic heart disease.
45
What are the causes of mitral regurgitation?
* Acute: MI and papillary muscle rupture * Chronic: Primary valve disease, secondary LV dilation
46
What are the symptoms of mitral regurgitation?
* Dyspnoea * Fatigue
47
What are the consequences of mitral regurgitation?
* Pulmonary oedema & PAH * Atrial fibrillation
48
ECHO classification in mitral regurgitation
- Regurgitant jet – severe >8cm2 , mild < 4cm2 - Pulmonary artery pressures measures
49
What are the options for mitral regurgitation repair?
* Open surgery * Transcatheter valve repair
50
When is open surgical repair of mitral regurgitation indicated?
* Younger, lower risk patients * Having open surgery for another procedure * transcatheter repair contraindicated
51
When is transcatheter repair of mitral regurgitation indicated?
* Old and frail * Previous sternotomy / chest wall deformity * Suitable valve anatomy
52
Compare overall outcomes for open repair of mitral regurgitation vs transcatheter
- Open = better MR reduction and more durable , longer hospital stay - Transcatheter = fewer complications, less invasive – can be done under local / sedation
53
Contraindications to open surgical repair of mitral regurgitation
- frailty , multiple comorbidities - chest wall deformities - previous sternotomy
54
contraindications to transcatheter repair of mitral regurgitation
- valve features o valve area too small < 3cm o leaflet length < 6cm o calcification at grasping area o thrombus / mass on valve o valve perforation - atrial access o small LA - endocarditis
55
What are the complications of transcatheter mitral regurgitation repair?
- bleeding – retroperitoneal bleeding, aorta , tamponade - TOE related injury – oesophageal perforation - Arrhythmias = AF most common - Pulmonary oedema – ASD, mitral stenosis - Device embolization – uncommon but serious neurological complication
56
What pre-operative planning is required before mitral regurgitation transcatheter repair?
- MDT approach – interventional cardiology, anaesthetist, echocardiographer, cardiac surgeon - Detailed pre op assessment – usually frail and need optimising - ECHO - Medications review – e.g. stop anticoagulants - Discussion with patient and family r.e. risks and consent
57
Describe the anaesthetic considerations / management for transcatheter repair of mitral regurgitation
- Remote anaesthesia – cath lab - TOE required - GA + intubation OR local + sedation - Arterial line - Defib pads attached - Haemodynamic goals maintained – reduce afterload, avoid bradycardia, Sinus rhythm etc
58
What are the haemodynamic goals required in mitral regurgitation?
- Reduce SVR / afterload – promotes forward flow - Maintain HR / avoid bradycardia – minimises regurgitation time and excess preload - Sinus rhythm – atrial contraction helps LV filling - Maintain contractility – supports forward flow – ionotropes - Avoid fluid overload - B agonists preferred over vasopressors – supports contractility and avoids high SVR
59
How can your anaesthetic help the surgeon in transcatheter MR repair?
- REDUCE LV SIZE o Easier for surgeons to grasp leaflets o Furosemide o PEEP – reduces pre load o Ionotropes – dobutamine , milronone - REDUCE MOVEMENT o Low TV 3-6ml/kg – help reduce heart motion to assist leaflet grasp o Avoid ventilatory changes when crossing atrial septum or when placing clips
60
Describe the transcatheter repair of mitral valve procedure
- Femoral access via seldinger - Heparin given - ACT 250-300 – prior to venous access - Transeptal puncture – TOE can guide position - Wire into LA , balloon dilated and clip delivery system advanced – using TOE - After procedure the atrial septal defect is assessed if significant shunting, it can be repaired - Final TOE – function and complications ## Footnote .
61
How are patients managed post op after transcatheter mitral regurgitation repair
- Most don’t need ITU - Pain is minimal - CXR – confirm clips and rule out pneumothorax / pulmonary oedema - Transthoracic acho within 24 hours – asses function / mitral stenosis - Restart anticoag
62
What is heart failure?
- Clinical syndrome in which heart is unable to pump sufficient blood to meet the metabolic demands of the body
63
What are common symptoms of heart failure?
* Breathlessness * Leg swelling * Fatigue * Poor exercise tolerance * Orthopnoea and paroxysmal nocturnal dyspnoea ## Footnote Symptoms can vary in severity and presentation.
64
What signs are indicative of heart failure?
* Elevated JVP * Pitting oedema * Basal crepitations on auscultation * 3rd heart sound ## Footnote These signs help in the clinical diagnosis of heart failure.
65
What are the positive investigation findings in heart failure?
* Raised BNP * Pulmonary oedema on CXR * Cardiomegaly on CXR * ECHO findings of reduced EF ## Footnote These findings are crucial for confirming heart failure diagnosis.
66
How can heart failure be classified?
* By side: left, right, congestive (both) * By ejection fraction: Reduced < 40% (HFrEF), Mildly reduced 40-50% (HFmrEF), Preserved >50% (HFpEF) o Improving = below 40% then increasing to >40% ## Footnote Classification aids in management and treatment strategies.
67
What are the stage of HF
- At risk – stage A – patients with HTN, T2DM, obesity, FHx of cardiomyopathy - Pre HF – stage B – without symptoms but evidence of 1 of the following – structural heart disease, abnormal filling pressures, elevated BNP - HF – stage C – symptomatic HF - Advanced – stage D – severe symptoms at rest, requiring hospitalisations, considered for advanced therapies
68
What disease processes result in HF
- HTN , IHD, valvular disease, myocarditis , HOCM, dilated cardiomyopathy
69
How are symptoms of LV failure classified
- NYHA = new York heart association - Class 1 = no symptoms - class 2 = symptoms on exertion, mild limitation - class 3 = symptoms on minimal exertion - class 4 = symptoms at rest
70
what signs of left sided HF are heard on auscultation of lungs
- crepitations at lung bases, 3rd heart sound, quiet lung bases (effusions)
71
How does HTN lead to LV failure
- increases afterload – LV hypertrophy – results in diastolic dysfunction and increased O2 demand - increased LV end diastolic pressure – reduces myocardial supply / perfusion - also close link between HTN and IHD
72
What are the common causes of right ventricular failure?
- intrinsic – infarction or cardiomyopathy - increased afterload o pulmonary HTN secondary too…  chronic hypoxic / COPD  mitral valve disease  P.E – acute / chronic  Drugs - Increased RV volume o LV failue o L to R shunt – ASD / VSD ## Footnote Understanding these causes is critical for targeted treatment.
73
Clinical signs of RV failure
- Pitting oedema - Hepatomegaly - Raised JVP - Ascites
74
How does a P.E lead to RV failure and LV failure
- P.E causes rise in pulmonary artery pressures – physical blockage and hypoxic vasoconstriction - This increases RV afterload and hence wall tension – increased RV O2 demand - RV cannot maintain this and will dilate - Can result in intraventricular septum bending towards LV - Reduced diastolic filling of LV and hence LV stroke volume = ventricular interdependence - Can result in reduced CO and coronary perfusion
75
What specific ECG and ECHO findings are in RV failure
- ECG o Pulmonary HTN – Right axis deviation, p pulmonale o RV ischaemia – ST changes I, III and aVF - ECHO o Loss of spherical shape o Increased RV:LV size ratio o Tricuspid regurgitation
76
What is the pathophysiology of HFpEF?
- Systemic inflammation results in microvascular endothelial inflammation and myocardial fibrosis – LV hypertrophy and stiffness - Results in Diastolic dysfunction - LV failure with reduced EF has systolic dysfunction = LV dilation ## Footnote HFpEF differs from HF with reduced EF as it primarily involves diastolic dysfunction.
77
What is the H2PEF score ?
- Scoring system to assess risk of HF in unexplained dyspnoea - BMI > 30, HTN, AF, PAH, > 60yrs, filling pressures - Score out of 9 = If score > 6 then likely HFpEF
78
Diagnosis of HF
- Symptoms and signs - BNP – raised - ECHO – EF – may be normal in HFpEF - Exclude other causes of breathlessness – anaemia, AF - Diagnostic toold – H2PEF score
79
What are the causes of falsely negative BNP
- Obesity , female, normal renal function, younger
80
How is HFpEF treated
- First line = SGLT2 inhibitor, diuretic + treatment of co-existing comorbidities - Non pharm = exercise rehabilitation, weight losss ## Footnote Effective management of HFpEF often requires addressing multiple health issues.
81
Why are SGLT2 inhibitors used in HF
- Diuretic effect – osmotic diuresis - Improve cardiac energetics – ketones - Anti inflammatory and hence anti fibrotic - Reduced hospitalisation and mortality
82
What are the perioperative risks associated with HF
- 4-6x increased mortality & morbidity - Cardiopulmonary complications - Non cardiopulmonary – AKI, strokes, sepsis
83
How would you conduct a pre op assessment in someone with HF
- Standard pre op ... - Focus on HF o exercise tolerance – subjectively (METS) or objectively (CPET) o Orthopnoea / PND o NYHA class ... - Detail on associated comorbidities – IHD, HTN, diabetes ... - Ix o FBC – anaemia exacerbates HF o ECG – arrhythmias o CXR ... - Cardiologist input in moderate/severe cases - Withhold SGLT 2 = 2-3 days before op
84
How many METS is considered high risk?
- < 4
85
How would you anaesthetise someone with HF
- maintain contractility by minimising anaesthetic depth where possible - induction - Smooth, slow, lower doses Coronary O2 - minimise O2 demand – avoid tachycardia - maintain MAP hypoxic pulmonary vasoconstriction – worsen RHF – normocapnia, avoid acidosis and hypoxia. Consider pulmonary vasodilators AABGI + arterial line +/- BIS Careful fluids
86
What increases risk of developing euglycaemic DKA from SGLT2 inhibitors
- Fasting - Surgical stress - Dehydration
87
How is the risk of euglycaemic DKA managed periop in elective and emergency surgery?
- If elective stop 2-3 days before, if emergency stop on admission - Monitor CBG and ketones in peroop period
88
How is euglycaemic DKA diagnosed
- Ketones >1.5 mM/l and pH < 7.3 and other causes of acidosis excluded
89
How is euglycaemic DKA managed?
- 10% glucose at 125ml/hr - Insulin 0.1units /kg/hr – i.e. treat as DKA
90
When are SGLT2 inhibtiors restarted after surgery
- After surgery when normal E+D and volume replete - If had episode of euglycaemic DKA – don’t restart, talk to diabetic team
91
What is a ventricular assist device (VAD)?
- A mechanical pumping device that helps to provide circulatory support. - Can be temporary or long term and used to support LV/RV/both - They are pre-load dependant and after load sensitive ## Footnote VADs can be temporary or long-term and support LV/RV/both.
92
What are the components of a VAD?
- Inflow cannula – ventricle - Outflow cannula – ascending aorta - Pump – sits in pericardial space - Controller / battery connected to pump ## Footnote Each component plays a crucial role in the device's function.
93
Give an example of a VAD device
- Heartmate 3 = 3rd generation = continuous flow centrifugal pump
94
How have the VAD devices improved with time?
- Today’s devices are continuous flow centrifugal pumps – lower incidence of pump thrombosis, stroke, GI bleeding - Previously pulsatile/ axial flow , more complications
95
What parameters can be altered on a VAD
- Flow rate = Cardiac output - Pulsatility index
96
What are the primary indications for a VAD
- Support whilst awaiting transplant - Long term for those ineligible for transplant - Temporary support bridging recovery after MI
97
What are major complications associated with VADs?
- GI bleed – continuous flow devices predispose to AV malformations plus anticoagulated. Common , up to 40% - Pump thrombosis - Stroke - Infections around the device ## Footnote Complications highlight the need for careful monitoring and management.
98
What anticoagulation is required for VAD
- INR 2-3 - Warfarin + aspirin (+/- clopidogrel)
99
What are the risks associated with surgery in those with VAD
- Usually co-morbid patients with poor CVS function - Potential for intra op VAD related complications - Anticoagulated - Mechanical ventilation can affect VAD functioning
100
Where should patients with VAD devices have surgery
- Specialist centre - Emergency surgery – close liaison with specialist centre
101
How would you assess someone pre operatively who has a VAD
* MDT approach – anaesthetist, cardiologist, VAD specialist nurse, other * Evaluating VAD function and any previous complications * anticoagulation status. * Assessing right ventricular function. / ECHO * Reviewing the patient's volume status and end-organ function and functional status * Standard pre op etc * Post op planning – ITU/ specialist centre
102
How is the VAD managed perioperatively
- Connect to an uninterrupted power supply - Care in movement and positioning - VAD specialist nurse present – monitor settings and function throughout - Place external defib pads on all patients
103
How do you manage the anticoagulation of someone with a VAD device?
- Stop warfarin 5 days pre op - Wait for INR < 2 then start IV heparin - Stop heparin 2-4 hours before surgery - Emergency surgery – reverse warfarin with prothrombin complex concentrate
104
What anaesthetic monitoring is recommended in those with VAD devices
- AABGI - Arterial line - CVP monitoring if large fluid shift / ionotropes requires - Consider TOE
105
What are the anaesthetic considerations/ adjustments in those with VAD
- Neuraxial usually contraindicated due to anticoag - Haemodynamic management o Preload dependant and afterload sensitive o Maintain MAP 60-80mmHg - Infection prevention o Strict asepsis for all procedures o Broad spec Abx inc antifungals - Bleeding risk o Patients have a von Willebrand deficiency due to pump degrading this o Desmopressin can help - Bipolar diathermy is preferred
106
How does intra op positioning affect pump function?
- Head up – reduces pre load and hence pump flow - Head down – increases pre load, can impair filling - Pneumoperitoneum – reduces pre load, increases after load – risk of suction event, inflate gradually
107
What are the risks of having a MAP >90mmHG in those with VAD
- Aortic regurgitation and pump thrombosis
108
What are the perioperative complications / emergency associated with VAD
- Pump thrombosis + blockage– due to stopping anticoag - Suction event - RV dysfunction – triggered by IPPV, hypoxia/ hypercarbia - Cardiac arrest
109
What is a suction event in those with VAD?
- The pump is dependant on preload and if there is inadequate preload it can cause LV to collapse and occlude the inflow cannula - Results in severe hypotension, ventricular arrythmias - Low flow alarm will sound - Caused by hypovolaemia, reduced venous return (pneumoperitoneum, Trendelenburg), RV failure, cardiac tamponade
110
How is a suction event managed
- Reduce pump speed - IV fluid bolus - Use ECHO to guide treatment
111
How do we manage a cardiac arrest in those with VAD
- Defibrillation and cardioversion are safe - Chest compressions are relatively contraindicated – can damage device – but if MAP < 50mmHg / EtCO2 < 20mmHg then necessary
112
What are the key post op considerations in those with VAD
- High care bed / cardiology - Monitor for bleeding - Restart warfarin after 1-2 days, bridge with heparin - VAD specialist nurse to check VAD function
113
List 4 categories of cardiac implantable electronic devices
- Pacemaker - Cardiac resynchronisation therapy device - Implantable cardiac defibrillator - Loop recorder – for investigating arrhythmias not detected by halter monitors
114
What are the indications for a permanent pacemaker?
* 3rd degree heart block * 2nd degree HB Mobitz type 2 * Unexplained syncope + bifascicular block * Symptomatic bradycardia ## Footnote These conditions warrant the need for pacing to maintain heart function.
115
What is cardiac resynchronisation therapy?
- Electrical implantable device with pacemaker and or defibrillator function that improves cardiac coordination and efficiency in severe HF - a form of biventricular pacing - Patients with HF often have dyssynchronous contractions between LV and RV and hence mechanical energy is lost and function is inefficient ## Footnote It addresses mechanical inefficiencies due to dyssynchronous contractions.
116
How are electrodes placed in cardiac resynchronisation devices?
- Passed into left subclavian vein - Right electrode passes through tricuspid valve - Left electrode passes through coronary sinus and into coronary veins to reach apex of LV
117
Indications for a cardiac resynchronisation device
- Symptomatic HF with LVEF < 35% despite optimal medical therapy with… o LBBB and QRS >130ms o QRS > 150ms o AF and QRS >130ms - Symptomatic AF with uncontrolled HR in patients who are candidates for ablation - Best result if QRS >150 and LBBB
118
What are the indications for an ICD?
- Primary prevention of life threatening arrhythmia = long QT, brugada , HOCM - Secondary prevention o Previous life threatening arrhythmia leading to cardiac arrest o Previous sustained symptomatic VT o Asymptomatic VT with HF
119
What aspects of a CIED should reprogramming be considered pre operatively
- Change response mode to asynchronous mode o this is if there is significant pacemaker dependency e.g. pacing spikes before most complexes. o This is because the pacemaker may misinterpret the diathermy as activity and stop pacing. - Advanced CIED functions may cause unhelpful rate changes periop o e.g. sometimes rate response uses minute ventilation to regulate pacing when sleeping / resting. Not appropriate perioperatively - Turn off ICD o switched off to eliminate risk of firing in response to electromagnetic interference if diathermy is used. o Attach external defibrillator pads - Disable any anti-tachycardia functions if diathermy used
120
State the reason for possible failure of arrhythmia management by a pacemaker in a patient having surgery that involves diathermy..
- Pacemaker interrupts the diathermy current as cardiac electrical activity and doesn’t generate an appropriate rate response
121
List 4 approaches to maximise the safety of intraoperative diathermy use in patient who have pacemakers for sinus bradycardia
- Asynchronous mode if very reliant on pacing - Bipolar diathermy - If monopolar needed, place the diathermy plate distant from pacemaker - Short rather than long bursts of diathermy
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List 2 non-pharmacological steps in the management of severe intraop bradycardia in a patient with circulatory compromise and no pacemaker response
* Transcutaneous pacing * Correcting cause e.g. electrolyte abnormalities, hypoxia, CO2, releasing surgical stimulus
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List 2 pharmacological steps in the management of severe intraoperative bradycardia.
* Atropine 500mcg * Glycopyrrolate 200mcg * Isoprenaline 5mcg/min * Adrenaline 2-10mcg/min
124
What is an intra-aortic balloon pump?
- Mechanical device that sits in aorta and inflates and deflates in counterpulsation with cardiac cycle. It is used to support cardiac function for those in severe HF, myocardial ischaemia or weaning of CPB.
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What is meant by counterpulsation and how does this improve LV function What does counterpulsation improve in terms of left ventricular function?
- Inflation in diastole and deflation just before systole - Inflation in diastole o Improves forward flow of blood and CO o Improves retrograde flow of blood and coronary perfusion - Deflation just before systole o Reduces LV afterload and wall tension – hence less O2 demand o Reduction in afterload also improves CO and allows forward flow of blood by heart - Overall .. o Improves coronary perfusion o Decreases myocardial O2 demand o Enhances cardiac output
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What is the equation for coronary perfusion pressure ? how does aortic balloon device effect this?
- Aortic diastolic pressure – LV end diastolic pressure - Aortic balloon Increases aortic diastolic pressure - Inflation of the pump may also stimulate NO release from endothelium and coronary dilation
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What are the indications for using an intra-aortic balloon pump?
- Acute HF with hypotension - MI with o papillary pupture + mitral regurgitation o acute LV failure o support needed during PCI - unstable angina while awaiting therapy – improves O2 blood supply and reduces demand - low CO after CABG / separation from CPB
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List contraindications of an intra-aortic balloon pump.
- Aortic disease o regurgitation – will promote this o dissection o aneurysm - uncontrolled sepsis - bleeding risk - tachyarrhythmias – cant synchronise with this - untreated PVD – could worsen perfusion
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What does an intra-aortic balloon pump consist of & where does it sit ?
- Balloon catheter inserted into aorta via femoral artery – fluoroscopic guidance - Sits in descending aorta , 2-3cm distal from subclavian artery - Distal end above renal arteries - Check position with Xray or TOE
130
List 2 methods of timing balloon inflation in IABPs.
- Arterial waveform o Inflation with dicrotic notch o Deflation just before upstroke of waveform - ECG o Inflation with T wave o Deflation with peak of R wave
131
Which method of timing balloon inflation is better in cardiac arrests?
- Arterial waveform because ECG no longer reliable e.g. PEA – false impression of cardiac output
132
Describe the arterial waveform when IABP is in use
133
What happens if there is mistiming of inflation of IABP?
- Inflates too early o Increases afterload and reduces intrinsic CO o Increases O2 demand o Potential aortic regurgitation - Late inflation o Suboptimal coronary perfusion and forward flow - Early deflation o Suboptimal reduction in LV afterload / O2 demand - Late deflation o Increases afterload and reduces intrinsic CO o Increases O2 demand
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What are the complications of inserting an IABP?
- Aortic damage o Dissection o Bleeding o False aneurysm - Infection - Thromboembolism – foreign body + pump promotes embolization - Bleeding related to anticoagulation - Thrombocytopenia and haemolysis - Blocked vessels by device o Worsening of PVD / compartment syndrome o Spinal cord ischaemia - Cardiac tamponade – dissection / rupture of aorta - Dyssynchrony - Balloon rupture and gas embolus
135
What gas is used to inflate the balloon of the intra-aortic balloon pump & why ?
- Helium - Low density = flow will be laminar to allow for rapid transfer from machine to balloon tip - Rapidly absorbed into blood in event of balloon rupture – minimises gas embolus risk
136
What is normal pulmonary artery pressure?
12-20mmHg.
137
Define pulmonary artery hypertension (PAH).
- Mean pulmonary artery pressure of 25mmHg or greater at rest or 30mmHg on exercise measured by right heart catheterisation - Recent guidelines suggest 20mmHg
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Who is idiopathic pulmonary hypertension more common in?
- Female > male - Patients with SLE, sickle cell
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What are the clinical features of pulmonary artery hypertension?
* Breathlessness * Exertional syncope * R side HF * Angina-like chest pain
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Cardiovascular consequences of chronic pulmonary HTN
- RH hypertrophy o Diastolic dysfunction o Increased O2 demand (plus increase EDV/P – reduces supply) - Increased pressure / remodelling – Tricuspid regurgitation - Eventually systolic dysfunction - Can lead to LV failure as RV size increases and septum deviates
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How is idiopathic pulmonary artery hypertension managed?
- Supportive = anticoagulation, diuretics, LTOT o Warfarin / DOACs as high risk of VTE / PE - Treatment = o CaCB – nifedipine, amlodipine o Endothelin receptor antagonist – bosentan o phosphodiesterase inhibitors = sildenafil o prostaglandins – inhaled iloprost - Definitive = lung transplant
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List 2 pharmacological agents which may be used in management of acute pulmonary HTN
- Reduce RV after load o Nebulised prostacyclin o Inhaled nitric oxide o IV sildenafil - Improve RV contractility o Ionodilator – milronone , levosimenden o Ionotropes – dobutamine, NA - Maintain SVR – metaraminol, NA, vasopressin - Optimise fluid balance – diuretics/ fluids
143
What are the anaesthetic implications of pulmonary artery hypertension?
* High risk mortality
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Anaesthetic goals in PAH
- Avoid increase in PAH / pulmnonary vasoconstriction – avoid hypoxia/ hypercarbia/ acidosis, hypothermia, pain , high airway pressures/ PEEP - Avoid fall in SVR – maintain coronary perfusion – invasive BP monitoring, pressors , cardiostable induction agents – fentanyl - Maintain sinus rhythm and contractility – avoid tachy (increases O2 demand and reduces diastole for coronary perfusion), ionotropes , minimise depressive effects of anaesthesia - Maintain optimum preload – avoid excess fluids – consider CO monitoring to guide this IPPV can worsen pressures and RV failure and decompensation
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Categories of PAH
- WHO classification 1. Pulmonary artery HTN - idiopathic, associated with systemic diseases e.g. HIV, drugs/ toxins or pulmonary HTN of new born. Remodelling of pulmonary vessels 2. LEFT heart disease 3. Chronic lung disease – COPD, OSA 4. Chronic thromboembolic disease 5. Other multisystem / unknown mechanisms
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What is atrial fibrillation (AF)?
Supraventricular tachyarrhythmia characterized by irregularly irregular ventricular contraction.
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What is postoperative atrial fibrillation?
AF that occurs within after surgery usually within the first week. - highest prevalence after cardiac / thoracic surgery e.g. CABG / valvular surgery - correlated with poorer outcomes, increased M&M, increased hospital stay, increase ICU need, overall hospital costs.
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What are the clinical features of AF?
- breathlessness, palpitations - syncope, chest pain - strokes - may be asymptomatic
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What are the causes of AF?
* Cardiac: HTN, valve disease, IHD, cardiomyopathy * Non-cardiac: thyrotoxicosis, alcohol, stress, electrolytes
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what is the ECG changes in AF
- loss of P waves - fibrillating/ irregular baseline - irregularly irregularly QRS complexes
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What are the risk factors for developing postoperative AF?
- Pre op = age, male, HTN, renal dysfunction, diabetes, high BMI , pre-existing CVS disease - Intra op = cardiac surgery – valve / CABG, use of bypass, long aortic cross clamp time - Post op = stopping B blockers / ACEi, electrolyte imbalance, critical illness / ITU
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what is the pathophysiology behind the development of post op AF
- stress response and sympathetic activation – increased catecholamines - Direct surgical irritation in cardiac surgery - electrolyte disturbances - arrhythmogenic - ischaemia from hypotension and anaemia and hypoxia - hypoxia / hypercarbia and increased pulmonary pressures and right atrial dilation
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What tools can be used to assess the risk of developing AF after surgery?
- CHA2DVASc (not just for assessing thrombosis and anticoag risk) - POAF = post op AF score
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What is the POAF score?
- Estimates risk of post op AF - Includes age, history of AF, male sex, HTN, COPD, CHF, valve surgery , LA enlargement - The higher the score, the higher the risk of post op AF
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What are the complications of developing postoperative AF?
- Thromboembolic – strokes - MI - Congestive HF - Risk of cardiac arrest - Risk of pneumonia - Increased hospital stay
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How can we minimize the risk of postoperative AF developing?
- Continue B blockers perioperatively - Optimise chronic illness / patient factors e.g. HTN - Intra op homeostasis – fluids, electrolytes, hypoxia/ hypercarbia - Steroid use - Regional anaesthesia / multimodel analgesia = reduces stress response
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How is AF managed
- Life style – caffeine, alcohol, weight loss - Rate control – B blockers, CaCB , digoxin - Rhythm control – electrical or pharmacological (amiodarone/ flecainide) - Ablation - Anticoagulation - Symptomatic unstable – DC cardioversion
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What comprises the CHADSVASc score?
* Congestive HF * HTN * Age >75 * Diabetes * Stroke * Vascular disease * Age >65 * Sex – female
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How would you preoperatively assess/ examine a patient with AF
- Assess if currently in AF – check pulse - Check if adequately rate controlled e.g. 60-80bom - Assessing for signs of HF - breathlessness / exercise tolerance / previous ECHO results / orthopnoe / pitting oedema/ pulmonary oedema - Medication history including use of anticoagulation - Potential causes of AF – goitre?
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State the mechanism of action of apixaban
factor Xa inhibitors
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How would you manage fast AF in theatre
- A to E, call for help, 100% O2 - 12 lead ECG - Reverse possible causes o Pain – opioids o Light anaesthetic o Anxiety – increase sedation if neuroaxial o Fluids if dehydrated o Rule out anaphylaxis, tension pneumothorax , LAST etc - If life threatening features o DC Cardioversion – 2joules/kg o Amiodarone 300mg IV over 15-20mins – if unsuccessful - Can also try o Valsalva o MgSO4
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The patient has normal renal function and planned to have spinal. How long should apixaban be stopped for?
48 hrs
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What pharmacological methods can manage broad complex tachycardia
- Amiodarone 300mg loading and then 900mg over 24 hours - MgSO4
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How do you manage a patient post cardioversion
- In recovery until fully awake / alert - 12 lead ecg + bloods
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What are the indications for emergency DC cardioversion ?
- Any life threatening signs – chest pain/ MI , syncope, heart failure , hypotension
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What is perioperative myocardial injury?
- Cardiovascular complication / injury after non-cardiac surgery within 3 days - Characterised by a rise in troponins indicating myocardial damage - No evidence of myocardial ischaemia - Associated with poor post op outcomes, increased M&M
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What is the difference between perioperative myocardial injury and myocardial infarction?
- MI o Rise in troponins plus one of  symptoms of MI  ECG changes associated with is ischaemia / LBBB  New regional wall motion abnormality on ECHO  Identification of thrombus on angio - Myocardial injury o Injury does not have evidence of ischaemia e.g. ECG changes / wall motion abnormalities etc o Can lead to infarction
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What are the different types of MI
- Type 1 = atherosclerosis - Type 2 = rate dependant - Type 3 = sudden death associated with MI
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What are the mechanisms for myocardial injury
- Reduced blood flow - Increased demand – e.g. tachycardia - Reduced O2 delivery – hypoxia , anaemia - Haemodynamic strain e.g. increased preload / afterload – catecholamines, fluids, IPPV
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What are the risk factors for myocardial injury?
- Age, male - Pre-existing risk factors – HTN, IHD, previous MI, HF, CKD - Emergency surgery - General surgery > ortho
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How can we prevent perioperative myocardial injury?
- Optimise CVS health pre op o Life style – smoking, alcohol, weight loss o HTN and diabetic control and statins o Correct anaemia o Continue aspirin and statins periop - Intra op o Avoid hypotension - Intra op hypotension, particularly systolic < 90mmHg has been associated with PMI o Avoid hypoxia o Avoid tachycardia - Post op o Good analgesia
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How is perioperative myocardial injury managed?
* Initiate statins and aspirin * No routine troponin checks in everyone post-op
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72 yr old man attends pre op clinic for robotic prostatectomy. He describes exercise induced chest pain. How would you assess him?
- HX o PMHx, DHx, allergies, smoking hx o Screen for signs and symptoms of IHD o Detailed exercise tolerance Hx o Nature and duration of pain, radiation o Chest pain at rest o Associated symptoms with the pain – dyspnoea, syncope, palpitations - Examination o CVS exam – heart sounds, pitting oedema, pulmonary oedema , JVP , HR and rhythm - Investigation o 12 lead ECG o Hb
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The patients ECG at rest is normal. How can we demonstrate inducible cardiac ischaemia
**- Exercise ECG** o Walking on tredmill increasing speed and incline gradually o Test stopped if blood pressure drops, ischaemic changes on ECG or patient symptoms o However not good for those who are limited to exercise for other reasons e.g. OA , limb amputation **- Dobutamine stress echocardiogram** o Baseline echo – ventricular function, valve function, ventricular wall motion abnormalities o Small IV dose of dobutamine o Assess echo – may identify regional wall motion abnormalities which indicate ischaemia **- CPET - Cardiac MRI**
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Describe features of anginal pain
- Central chest pain - May radiate to left arm / jaw - Crushing / tightness in nature - Triggered by activity, Relieved by rest
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What is the pathophysiology of angina
- Atherosclerosis of coronary vessels resulting in narrowing - During times of exercise, blood flow does not meet the increased O2 demand of heart - May be stable – fixed stenosis, cant dilate to meet demand, relieved by rest - Unstable – increased frequency or at rest – caused by plaque rupture and sudden decrease in coronary flow but not full occlusion - Vasospasmic angina – epicardial artery vasospasm e.g. cocaine
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Pathophysiology of ACS
- Atherosclerosis - Plaque rupture - Thrombosis - Myocardial ischaemia - Infarction
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What are the risk factors for coronary artery disease?
Non-modifiable: Male, Age, Family History. Modifiable: Smoking, Hypertension, Hyperlipidaemia, Diabetes, Obesity. ## Footnote Addressing modifiable risk factors can help in prevention strategies.
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How can angina severity be classified?
* Class 1: Occurs only during strenuous exercise * Class 2: Mild dyspnoea/angina in moderate exercise * Class 3: Marked limitation to activity due to pain/dyspnoea, comfortable at rest * Class 4: Angina/dyspnoea even at rest ## Footnote This classification helps in the management and treatment of angina.
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Why is cardiac pain referred to the left arm or jaw?
- The heart is innervated by T1-T4 sympathetic fibres - Visceral afferents fibres of the heart are transmitted via these sympathetic paths - Sensory somatic afferents from T1 – T4 dermatomes (arm and shoulder) also synapse at these levels of the dorsal horn - Brain interprets the visceral afferents of the heart as the T1-T4 somatic dermatomes ## Footnote This phenomenon is known as referred pain.
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What is the most common cause of death after acute coronary syndrome (ACS)?
Cardiogenic shock. ## Footnote This condition results from inadequate blood flow and can lead to multiple organ failure.
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Most common arteries affected by ACS
- LAD then RCA then left circumflex
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What is the management protocol for a STEMI according to NICE guidelines?
- Immediate = MONA – morphine, oxygen, nitrates (GTN), aspirin 300mg - < 120 mins since presentation = PCI + DAPT - > 120 mins = thrombolysis +/- rescue PCI - Anticoagulation during PCI = unfractionated heparin +/- GPIIb/IIIa inhibitor (abciximab / tirofiban) - DAPT = aspirin + P2Y12 inhibitor (clopidogrel) = 12 months ## Footnote DAPT refers to dual antiplatelet therapy, typically aspirin and a P2Y12 inhibitor.
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How is NSTEMI managed?
- MONA - Fonduparinux (factor Xa inhibitor) – unless bleeding risk / immediate PCI planned - Aspirin + Clopidogrel - Risk stratification using GRACE score – if high then angiography +/- PCI
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What is Wolf-Parkinson-White syndrome?
A type of AV re-entrant tachycardia due to an accessory pathway between the atria and ventricles. ## Footnote This condition can lead to rapid heart rates and is associated with specific ECG changes.
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What are classic ECG findings in WPW?
* Delta waves * Short PR interval ## Footnote These findings are characteristic of the accessory conduction pathway in WPW syndrome.
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What is the issue of WPW and AF
- Accessory pathway allows fast conduction of depolarisations - Can lead to VF
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How are patients with WPW managed anaesthetically
- Avoid sympathetic stimulation – can result in AVN re-entry tachy o avoid ketamine o good analgesia - avoid glycol/atropine - avoid neostigmine – blocks AVN and promotes accessory pathway
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Define cardiogenic shock.
- Inadequate circulatory function resulting in organ hypoperfusion and tissue hypoxia as a result of cardiac dysfunction - Clinical parameters o Persistent hypotension = systolic BP < 80-90 / MAP < 30mmHg o Cardiac index < 1.8 L/min/m2 unsupported with adequate LVEDP (filling pressure) o Clinical signs = cool peripheries, confusion, oligouria o LAB results – lactic acid, high creatinine ## Footnote This condition is often a result of severe myocardial infarction.
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what is the pathophysiology of cardiogenic shock after ACS
- Thrombosis of coronary vessel results in LV ischaemia / infarction and ultimately dysfunction - Reduced contractility – hence lower CO + hence lower MAP - LVEDP increases as a result o worsens coronary perfusion o Pulmonary oedema and hypoxaemia - Additionally to pump failure o Neurohormonal activation – RAAS + sympathetic o Vasoconstriction and fluid retention – further tissue hypoperfusion o Vicious cycle as now more circulating volume – increased EDP + pulmonary congestion - Hypoxia, acidaemia etc
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How would you assess someone potentially in cardiogenic shock?
- Hx - Examination - IX = bloods, troponins, pH/lactate, renal , urgent ECHO
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What are the ECHO findings in cardiogenic shock post MI
- Regional wall motion abnormality - LV / RV dysfunction - Valve dysfunction
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How is cardiogenic shock after ACS classified?
* A: At risk * B: Beginning * C: Classic CS * D: Deteriorating * E: Extremis (e.g. cardiac arrest) ## Footnote This classification aids in determining the severity and management approach.
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What are the phenotypes of cardiogenic shock?
- All have reduced CO however SVR and wedge pressure varies o Wet and cold – high SVR (cool peripheries) pulmonary congestion and increased pulmonary capillary wedge pressure o Cold and dry = high SVR, low PCWP o Wet and warm = low SVR, high PCWP ## Footnote These phenotypes help guide treatment strategies based on hemodynamic profiles.
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What is the management for cardiogenic shock after MI?
Revascularization and reperfusion through PCI or surgical revascularization. ## Footnote Timely intervention is critical to improve outcomes in cardiogenic shock.
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When is surgical intervention for cardiogenic shock secondary to MI needed?
- When PCI not successful in revascularization - Valve repair e.g. acute severe mitral regurgitation - Ventricular septal rupture
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How are patients supported in the interim whilst awaiting revascularisation / management after ACS and cardiogenic shock . how do these help?
**- Mechanical circulatory support (MCS devices)…** o Intra aortic balloon pump= increases coronary perfusion, some CO support, reduces LV afterload o Left Ventricular assist device = impella = Higher CO support, reduces LV wall stress and myocardial O2 demand o VA- ECMO= Strong CO support however can increase LV afterload **- Ventilatory support** o CPAP o Invasive ventilation may be required to support before and to facilitate procedure
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What are the benefits of mechanical circulatory support devices?
- Boost CO and hence organ perfusion - Reduce amount of catecholamines needed - improve myocardial O2 supply / demand balance ## Footnote These devices can provide temporary support while awaiting definitive treatment.
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What are the pros and cons of invasive positive pressure ventilation (IPPV) in cardiogenic shock?
- Pros = o maximise oxygenation – can add PEEP, max FiO2, lung recruitment o reduces LV afterload (uncoupling of LV) o reduces venous return and pre load for those overloaded - Cons = o reduces venous return which may be a problem in those deplete o reduces RV output due to higher pressures o requires sedation / anaesthesia which has negative cardiac ionotropic effects ## Footnote The use of IPPV must be carefully considered in the context of the patient's hemodynamic status.
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how is circulation managed in someone with cardiogenic shock
- avoid excess fluids for resuscitation - noradrenaline 1st line o ionotropy and vasoconstrictor o titrate careful to prevent excess LV afterload - ionodilators – reduce afterload whilst improving contractility o milrinone and levosimenden - Ionotropic agents – dobutamine ## Footnote It is titrated carefully to prevent excess LV afterload.
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How can we monitor someone with cardiogenic shock
- Arterial line for invasive BP monitoring and taking regular gas’s - ECHO – cardiac output and function and can guide changes to ventilator setting / vasopressors - Pulmonary artery catheterization – detailed haemodynamic
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Other than ventilatory and CVS support, what other support may patients with cardiogenic shock require
- Sedation – to facilitate ventilation, reduce O2 demand - Renal – AKI is very common , monitoring U&E, ?dialysis - Hepatic – monitor LFTs , hepatic dysfunction can occur from congestion - GI ulcer prophylaxis + DVT prophylaxis - Haematological – Hb target of 90-100 g/L
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Why may patients with cardiogenic shock after ACS need intubation?
- Improve oxygenation - Improve haemodynamics – reduces LV afterload and reduces pre load - Facilitate surgery / intervention
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What are the anaesthetic concerns in someone undergoing PCI in cardiogenic shock
- Often conscious sedation o Risk of airway loss o CVS instability - May need GA o Slow induction – low cardiac output states delays onset of anaesthesia o High dose fentanyl and reduce propofol - Remote site anaesthesia - Post op ITU arranged – high risk of MoF and usually need some period of stabilising before extubating
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What drugs improve cardiac contractility – name and mechanism
- Levosimenden = calcium sensitiser, improves Ca binding to troponin C , opens ATP K+ channels – vasodilation = ionodilator - Milronone = phosphodiesterase 3 inhihibitor – reduces breakdown of cAMP – more Ca influx - Dobutamine = B1 agonist – increases cAMP – more Ca influx - Digoxin = inhibits Na/K ATPase – increase in intracellular Na drives Na/Ca exchanger – more Ca
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What is the definition of vasoplegic shock?
- Sustained hypotension and organ hypoperfusion as a result of pathological vasodilation - Characterised by increased vasopressor requirements, organ hypoperfusion and capillary leak Sustained hypotension and organ hypoperfusion due to pathological vasodilation. ## Footnote This condition can occur in various clinical settings, including sepsis and anaphylaxis.
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List the causes of vasoplegic shock.
* Anaphylaxis * Sepsis * Burns and trauma * Pancreatitis * Spinal cord injury * Neurogenic shock * Spinal anaesthesia * Cardiopulmonary bypass ## Footnote Identifying the underlying cause is crucial for effective management.
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What causes vasoplegic shock in CPB?
- blood contact with extracorporeal circulation sets up SIRS response. - Also tissue injury and reperfusion injury ## Footnote Severe hypertension can have wide-ranging effects on multiple organ systems.
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Risk factors for developing shock after CPB?
- Impaired heart function - Extended bypass time - Use of pre op ACEi / ARBs
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Describe the pathogenesis of vasoplegic shock…
**- Systemic inflammation** o PAMPS – pathogen associated molecular patterns = Lipopolysaccharide and porins) o DAMPS - damage associated molecular patterns (DNA, ATP) o Results in cytokine release **- 4 main mechanisms** o Vasodilation = cytokines trigger NOS – smooth muscle relaxation o Vascular responsiveness = high levels of catecholamines and angiotensin leads to receptor down regulation. Acidosis activates K+ ATP channels – hyperpolarisation. Overall smooth muscle relaxation o Microcirculatory dysfunction = capillary leak from damaged glycocalyx. microthrombi formation and impaired blood flow o Cellular hypoxia and mitochondrial dysfunction
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How does vasoplegic shock present
- Hypotension – with low diastolic pressure - Warm peripheries - Bounding pulse – often tachycardic - Prolonged cap refil
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How does vasoplegic shock effect MAP, CO, SVR
- Low MAP, low SVR, high CO
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How can cardiac output be monitored in vasoplegic shock
- Pulmonary artery catheter – gold standard but uncommon - ECHO - PiCCO and LiDCO - using arterial line + central catheter
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How is vasoplegic shock managed?
- Fluid resuscitation – monitoring for fluid responsiveness to prevent overload - Vasopressors – o Noradrenaline = 0.05-0.1 ug/kg /min - If there is catecholamine refractory shock e.g norad >0.2ug/kg/min o Start vasopressin 0.02 – 0.04 units / min o Others adrenaline, dopamine, methylblue o Often multi model strategy required due to receptor insensitivity / down regulation - Hydrocortisone 200mg / day - Treat underlying cause e.g. sepsis - Constant re-evaluation of MAP, end organ function, lactate and cap refil
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Are there any adjuvant therapies for vasoplegic shock
- Corticosteroids – hydrocortisone +/- fludrocortisone
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What is the outcome of high dose vit C in sepsis
- Not recommended , adverse events
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What is a normal cardiac index reading found on cardiac ouput monitoring
- 2.5-3.5 L/min / m2 - Higher in vasoplegic shock
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How might LV ejection fraction change in vasoplegic shock
- Higher because of lower CO
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Define a hypertensive emergency
- Presence of acute HTN + organ damage – heart , retina, kidneys , brain
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Define a hypertensive urgency
- Acute HTN without organ damage
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Define severe HTN
- >180/110mmHG
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What are hypertensive crisis?
- Hypertensive emergencies and urgencies
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What are the causes of hypertensive crisis?
- Aortic dissection - Pheochromocytoma - Ischaemic stroke - Subarachnoid haemorrhage - Drug related – cocaine, MAO inhibitors + tyramine rich foods - Pre eclampsia
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What are the systemic effects of severe HTN
- Respiratory = pulmonary oedema - Neuro = o altered consciousness o encephalopathy (seizures, lethargy, coma) o posterior reversible encephalopathy syndrome (PRES) o stroke - renal dysfunction - CVS: o Arrhythmias o myocardial ischaemia (increase afterload and myocardial O2 demand and vasospasm)
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How is severe HTN investigated?
- BP all 4 limbs - Look for end organ damage o 12 lead ECG , troponin o Fundoscopy – papilledema, retinal haemorrhages o U&Es , urine dip , urine albumin: creatinine o CXR - Cause o CT angiography aorta o Urinary catecholamines / meteniphrines o Pregnancy test
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How are hypertensive crisis managed?
- Control BP o Usually require rapid control within 1 hr e.g. ACS, pulmonary oedema, aortic dissection, pre-eclampsia and pheochromocytoma crisis o Try avoid bolus’s and use steady infusions o Avoid hypotension - Treat underlying cause
227
Options for anti-hypertensive agents used in hypertensive crisis - doses and side effects
228
Other than HTN crisis when else is BP management important / targeted
- Post op if bleeding is a concern o carotid endartectomy – risk of rebleed / haematoma / cerebral hyperperfusion syndrome o Aortic surgery – strict target to prevent aortic injury but maintain spinal cord perfusion o cardiac surgery – HTN can compromise suture integrity – vessel rupture, tamponade - Neurological conditions – acute ischaemia stroke , acute intracranial haemorrhage - Major bleeding / major trauma
229
What are the blood pressure targets for different causes of hypertension?
* ACS: Systolic < 140 * Aortic syndromes: Systolic < 120, HR < 60 * Pre-eclampsia: < 160 * Pheochromocytoma: Systolic < 140 ## Footnote These targets are important for managing specific hypertensive crises.
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First line anti HTN agents used in malignant hyperthermia, acute pulmonary oedema, pheochromocytoma crisis, ACS, acute aortic syndrome and pre-eclampsia
- ACS = IV nitrates and labetolol (plus IV opioids for pain) - Acute pulmonary oedema = GTN - Acute aortic syndromes = esmolol / labetolol - Pheo = phentolamine - Pre-eclampsia = MgSO4 , labetolol
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What is infective endocarditis (I.E)?
Infection of cardiac endothelium that can result in significant systemic complications
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What organism cause infective endocarditis?
- Main one = S.Aureus - associated with IVDU or invasive proceeedures - Also o Steptococcus viridans – subacute – linked to oral cavity o Enterococcus faecalis – GI and GU procedures o Streptococcus bovis – GI malignancy o Coagulase neg staphylococcus e.g. epidermidis = prosthetics valves o MRSA, fungal , HACEK organisms S. Aureus - associated with IVDU or invasive procedures
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What are the risk factors for infective endocarditis?
* Cardiac: CHD, prosthetic valve/implantable device, bicuspid valve, rheumatic fever, previous I.E * Non-cardiac: IVDU, poor dentition, immunocompromised, diabetes, malignancy, > 65 years, long-term venous device, haemodialysis
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Is infective endocarditis more common in males or females?
Males
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What causes the pathogenesis of infective endocarditis?
- Turbulent flow can cause trauma to endothelium - Sets up platelet activation and coagulation cascade – sterile vegetation forms on surface of endothelium - Transient bacteraemia can attach to this and grow
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What are the complications of infective endocarditis?
- Cardiac o Valve regurgitations – HF, pulmonary oedema, shock o AV node conduction defects e.g. aortic root abscess o AF o Perivalvular abscess and fistula formation - Sepsis - Renal o Septic emboli – AKI and glomerulonephritis , also caused by sepsis - CNS o Septic emboli – strokes - Septic emboli can also infarct liver, spleen, limbs abscess and fistula formation
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What persistent infections in infective endocarditis are caused by?
Resistant organisms, abscess, larger vegetations lasting > 7-10 days despite antibiotics requiring surgical intervention
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How does infective endocarditis typically present?
- New onset Murmur + fever - Systemic – weight loss, malaise, fatigue - Sepsis - Clinical signs = Janeway lesions, oslers nodes, splinter haemorrhages - Other features / complications – AKI, pulmonary oedema, cognitive changes etc
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How is I.E diagnosed?
- DUKES criteria - 2 major OR 1 major 3 minor OR 5 minor - Major = o 2x positive blood cultures of typical organism o ECHO or CT findings consistent with I.E- vegetation, abscess, new valve lesion - Minor o Risk factor o Fever >38 o Vascular phenomena – emboli, Janeway lesions, intracranial lesions o Immunological phenomena – oslers nodes, roth spots o Microbiological evidence that is not in keeping with major criteria
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What is the first-line imaging for diagnosing infective endocarditis?
Transthoracic echocardiogram - TOE more sensitive – can be done if transthoracic is inconclusive
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What is the treatment approach for infective endocarditis?
- MDT approach – IDU, cardiologist, critical care, other organ systems involved, surgeons - A to E resuscitation - IV Abx – ideally after cultures o 4-6 weeks o Choice depends on micro and pt hx and native or prosthetic valve o E.g. native valve = amoxicillin + gentamicin o E.g. native valve pen allergy = vancomycin + gentamicin o E.g. prosthetic = Vancomycin, gentamicin and rifampicin o I would use trusts local microbiology guidelines
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Which antibiotics are used for MRSA in infective endocarditis?
Vancomycin OR daptomycin
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What are the indications for surgery in infective endocarditis?
* Large vegetations > 10mm post embolization/valve dysfunction OR > 15mm * Infection of prosthetic material * High embolic risk * Severe valvular regurgitation * Uncontrolled infection/persistent infection
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Pre op considerations prior to I.E surgery
- Standard pre op - MDT planning – other organs involved - Assess complications – renal, CNS , HF , arrhythmias, coagulopathy – correct and optimise - Ensure effective Abx dose and type started - Review imaging – TOE / ECHO findings - Consent and risk discussion - Organise ITU bed post op
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Describe intra op anaesthetic management of I.E patient…
- Monitoring – AABGI + Arterial line + central venous access + continuous TOE - Maintain haemodynamics – vasopressors / iontropes – guided by CO monitoring
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What are the poor prognostic indicators of infective endocarditis?
* Patient factors: older, prosthetic valves, diabetic * Clinical features: stroke, shock, heart failure, renal failure * Microbiology: S. Aureus, fungal * ECHO: severe regurgitation, large vegetation, abscess, low EF
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How does infective endocarditis present in intravenous drug users (IVDU)?
- Right side of heart – tricuspid valve – murmur 4th intercostal left sternal border, systolic murmur - Pneumonia and septic P.E - Same as before – fever, malaise, weight loss Right side of heart - tricuspid valve - murmur at 4th intercostal left sternal border, systolic murmur, pneumonia, and septic pulmonary embolism
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What conservative measures can help avoid infective endocarditis?
* Good aseptic care of wounds * Good oral and skin hygiene * Avoid tattoos and piercing * Avoid central lines where possible
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When is antibiotic prophylaxis indicated for infective endocarditis?
- Those at high risk undergoing high risk procedure - E.g. prosthetic valve, previous I.E, cyanotic CHD , HOCM - High risk procedure – certain dental procedure e.g. dental extraction or perforation of oral mucosa
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Which antibiotics are given for prophylaxis of infective endocarditis?
- 30-60 mins before procedure - Amoxicillin OR clindamycin in pen allergy
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What is heparin?
Naturally occurring glycosaminoglycan with a molecular weight ranging from 3-30kDa, can be unfractionated or fractionated
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What is the primary action of heparin?
- Potentiates the breakdown of factor Xa and thrombin by antithrombin 3 by binding AT3 - LMWH has minimal thrombin inhibition but potentiates breakdown of factor Xa - At high doses heparin also acts a tissue factor pathway inhibitor independent of ATIII
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What are the limitations and side effects of heparin?
- Unfractionated has variable effects - Heparin response varies in individuals and risk of heparin resistance - Side effects o Bleeding o Heparin induced thrombocytopenia o Hyperkalaemia o Hypotension – histamine release at hight doses
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How is heparin reversed?
With protamine, a cationic protein that binds heparin and neutralizes it
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What are the side effects of protamine sulphate?
* Hypotension / haemodynamic instability – most common can be minor or severe * Pulmonary HTN * Anaphylaxis * Risk of bleeding if ratio not correct… - Unbound protamine inhibits platelet activity, adhesion and aggregation - bleeding - downregulates other clotting factors - Enhances fibrinolysis - activates tissue plasminogen activator
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What is heparin resistance?
Inadequate response to heparin despite adequate dose, with ACT <480 despite 300-400 units/kg
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What are the causes of heparin resistance?
* ATIII deficiency - Congenital – auto dom - Acquired – liver failure (reduced synthesis), nephrotic syn (increased clearance), DIC, recent use of heparin. * Increased heparin clearance * Elevated heparin binding proteins – I.E / sepsis , malignancy * Haemodilution e.g. extra volume in CPB , dilutes heparin / ATIII * Hypothermia – reduces ATIII activity and hence heparin function
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What operational causes are there of inadequate anticoagulation after heparin administration
* Administration error – not flushed through, cannula tissued , wrong drug
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How is heparin resistance managed?
* Repeat heparin dose * Give ATIII – FFP or recombinant ATIII concentrate * Give other anticoagulants if persistent = Bivalirudin
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What is heparin pseudoresistance?
* False impression that patient is not responding to heparin however actually due to another reason e.g. other factors – elevated fibrinogen / factor 8
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What is heparin rebound?
* Residual heparin post op and risk of bleeding * Caused by incorrect protamine dosing or poor clearance of heparin
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How is the residual heparin amount determined?
* Can measure ACT and then add heparinase and compare ACT – helps differentiate the ACT from other coagulation issues * However ACT not that accurate * Could technically do a anti-Xa assay (heparin assay) but this takes time so not practical
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What is the activated clotting time test?
* Point of care test used in cardiac surgery to assess coagulation * Uses kaolin or celite = surface reactor that activates clotting pathway * Measures time taken to clot * The longer the time, the less coaguable
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What are the options for point of care/ lab tests to determine effectiveness of heparin in cardiac surgery – advantages and disadvantages of each
265
How do prothrombotic disorders affect anticoagulation for cardiac surgery?
* Antiphospholipid syndrome - Autoantibodies activate endothelial cells and platelets – arterial / venous thrombosis - APTT and ACT often elevated at baseline and cause monitoring difficulties * Factor V leiden - Mutation in factor 5 and resistance to protein C - No effects on heparin, protamine and ACT monitoring * Protein C and S deficiency - No effects on heparin, protamine and ACT monitoring * Haemophilia - X linked recessive – factor 8 or 9 deficiency - Replace factors pre op to normalise pre op in vitro clotting tests - Then use heparin and ACT monitoring as normal
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What is HIT and the different types?
Complication of heparin administration * Type 1 and 2 * Type 1 = mild thrombocytopenia and resolves upon discontinuation , presenting 2-3days after heparin exposure , non immune mediated (direct platelet activation by heparin). * Type 2 = immune mediated platelet destruction, severe thrombocytopenia, presenting 5-14 days after administration.
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How does type 2 HIT develop
* Immune complexes between heparin , platelet factor 4 and IgG * Autoimmune destruction of platelets and endothelial damage
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Define thrombocytopenia
- Platelet count < 150 x 10^9 g/l
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What are the risk factors for HIT?
* High dose >32,000 units * Pre/post op continuous infusions * > 4 days * IV route > SC * Female * Unfractionated > LMWH
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How is HIT diagnosed?
* 4 Ts - Thrombocytopenia - >30% drop - Timing of platelet fall – onset 5-10 days - Thrombosis – new DVT / PE / skin necrosis - Likelihood of other causes of thrombocytopenia * Total of 8 points, if >/=4 then high risk * If high risk = ELISA ab screening – immunoassay
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2 features that suggest HIT in ITU patient
- Sudden significant platelet drop - Thrombosis while on heparin
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Complications of HIT type 2 in ITU
- Arterial Thrombosis – MI, strokes, PVD - Venous thrombosis – PE - Local skin necrosis - Systemic – fever etc
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What is the management of HIT in those needing cardiac surgery?
* Post pone non urgent surgery until resolves >100days * Urgent procedure – use other agents - Direct thrombin inhibitors = Bivalirudin preferred, other option argatroban - Factor Xa inhibitor = fondaparinux - not ideal as long half life - Danaparoid – not in UK - OR plasmapheresis to remove IgG
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What are the disadvantages of bivalirudin and argotroban as anticoagulants for CPB?
* No specific reversal agent * ACT non linear and less reliable * Prolonged effect in renal failure
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Other causes of thrombocytopenia
- Consumptive – DIC - Dilutional - Decreased production – chemo - Sequestration – splenomegaly - HIT
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What is CPB?
- Extracorporeal circulation used to support heart during cardiac surgery - Provides both pumping support and oxygenation - Allowing a bloodless motionless field for surgery
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Define extracorporeal circulation
- Any process whereby blood volume is circulated outside the body
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What are the components of the CPB circuit?
- Venous reservoir o Collects blood from heart = Via cannula into right atrium / vena cava o Blood can also be collected from various surgical salvage devices / suction - Pump o An arterial pump then pumps blood from a venous reservoir too… o a heat exchanger and oxygenator - Splitting of blood stream o A fraction of the blood is combined with cardioplegia solution and then reintroduced into the coronary circulation proximal to the aortic cross clamp o The remainder passes through an arterial filter and is returned to the systemic circulation
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Which vessels are cannulated in CPB?
- Venous o RA, SVC, IVC o Sometimes femoral for minimally invasive or emergency CPB - Arterial o Ascending aorta o Subclavian artery – if aorta diseased o Femoral artery – minimally invasive surgery
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In what ways can we manipulate CPB circuit
- Gas exchange o Increase FiO2 on membrane oxygenator o Increase gas flow to remove CO2 - MAP o Increase CPB flow rate – increases MAP o SVR manipulated pharmacologically - Temperature o Via heat exchanger - Haematocrit o Volume added / removed via ultrafiltration - Acid base management o pH stat or alpha stat methods
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What is the difference between the pH stat and alpha stat methods of acid-base management in CPB?
- pH stat = constant pH regardless of temp change o add CO2 to maintain pH as temp changes o cooling increases pH so CO2 added to maintain pH o CO2 will increase cerebral blood flow and improve cerebral cooling and O2 delivery - Alpha stat = pH rises with cooling during CPB o Allows for alkalosis during cooling as more physiological for protein ionisation and autoregulation maintained.
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What is cardioplegia?
- Solution added to coronary vasculature to support heart and surgery during CPB - Achieves intentional and temporary diastolic arrest and myocardial protection
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What are the different types of cardioplegic solution
- Cold crystalloid – 4 degrees - Cold blood – 4 degrees - Warm blood
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What is the advantage of cold cardioplegic solutions
- Reduce O2 demand and metabolism – protects against ischaemia
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Examples of substances in cardioplegic solution and their purpose
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What are the two routes for delivering cardioplegic solution?
- Proximal to the aortic cross clamp - And thus delivered to heart o Anterograde via aortic root and coronary ostium (arteries) = dependant on adequate root pressure, coronary artery perfusion and competent aortic valve o Retrograde via coronary sinus (venous) – e.g. if significant coronary artery occlusion
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What are the purposes of cardioplegia in cardiac surgery?
- Facilitates surgery o Motionless relaxed heart – K+ creates state of diastolic arrest o Bloodless field - Myocardial protection o Diastolic arrest – reduces metabolic demand o Cooling of heart – reduces metabolic demand o Blood can be used to improve O2 delivery * Facilitates surgery * Motionless relaxed heart * Bloodless field * Myocardial protection * Reduces metabolic demand
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What are the complications of cardioplegia solutions?
- Direct vessel damage during cannulation o Bleeding o Embolic strokes - From solution o Haemodilution – anaemia / thrombocytopenia o Overload o Electrolyte distubances o Air embolus – coronaries or systemic - From infusion o High pressure – oedema , coronary rupture o Non uniform spread – areas of warm ischaemia
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What non-cardioplegic techniques are there?What is the intermittent aortic cross clamp technique?
- Intermittent aortic cross clamp o Clamped to stop blood flow – brief period of ischaemia o Unclamp – reperfusion and oxygenation o Repeated to limit injury to myocardium - Fibrillation technique o VF induced to prevent contraction and then cardioverted to prevent ischaemic damage - Off pump cardiac surgery
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What are the issues with intermittent aortic cross clampa and fibrilation techniques
- Intermittent aortic cross clamp o Reperfusion injury and damage o May dislodge atheroma o However useful for short procedure and avoids cardioplegia - Fibrillation technique o Ongoing O2 demand – risk of ischemia during fibrillation o Risk of embolization o May not be able to revert to sinus
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What are the risks of CPB?
- Intraoperative o Circuit clotting o Bleeding associated with anticoagulation / consumptive coagulopathy / platelet dysfunction o Haemolysis o Aortic dissection o Gas embolization - Post op o SIRS o Renal dysfunction – overload/ AKI/ electrolytes o Neurological – post op cognitive dysfunction and stroke due to hypoperfusion or emboli
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How can neurological damage post-CPB be minimised?
- Adequate perfusion pressures - Normoglycaemia - Normothermia - Cerebral oximetry in high risk - Confirmation of de-airing by surgeons
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What are the risk factors for embolic event in CPB?
- Age - Aortic atheroma - Previous stroke - Diabetes - Surgical factor – valve replacements
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What are the roles of an anaesthetist during CPB?
- Anticoagulation – heparin, ACT and protamine - Temperature management – falls in bypass , ensure normalisation before coming off bypass - Acid base / electrolytes – normalised before coming off bypass - Maintain anaesthesia – TIVA / volatiles via CPB circuit - Maintain haemodynamic and cerebral perfusion pressure – vasopressor support , closely work with perfusionist - Coordination with surgeon / perfusionist when coming off bypass o Lungs re-expanded and ventilated o Heart progressively filled by clamping venous line and giving boluses
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What happens to temperature during CPB?
- May use o Normothermia o Hypothermia – 25-32 degrees o Deep hypothermia – 15-18 degrees - Drop in temp to reduce O2 consumption and risk of ischaemia. Plus cerebral protection - However risk of coagulopathy and impaired protein / membrane function
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What is the reason for anticoagulation during CPB?
- Extracorporeal circulation with artificial surface – activates clotting cascade - Vessel injury during cannulation – coagulation activated - Anti coagulation offsets this and prevents clot formation and circuit failure / strokes etc
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Describe how you would anticoagulated for CPB
- 300-400units / kg heparin IV - total body weight - Wait 3-8 mins and check ACT - Aim for ACT >480 seconds before starting CPB - Recheck ACT every 30 mins - Repeat 1/3 dose of heparin after 90 mins then every 60 mins - Adjust in renal failure
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How is heparin reversed + doseHow is heparin administered for CPB?
- Protamine sulphate - 1mg / 100units of heparin given - Infuse over 15 mins
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What is the significance of the protamine:heparin ratio?
* Dosing of protamine should be based on the heparin concentration * Should aim to give a protamine: heparin ratio of 0.6- 0.8 * If >1.3: 1 then risk of bleeding due to platelet dysfunction (from excess protamine) * If <0.6 then bleeding risk due to excess heparin
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Similarities and differences between ECMO and CPB
- Both extracorporeal circulations used to support ventilation and cardiac function - However ECMO o Uses peripheral vessels o Longer term use – circuit is more biocompatible and membrane oxygenator is longer lasting o Centrifugal pump – gentler - CPB o Central vessels o Short term use o Roller pump – harsher on blood – higher flows but haemolysis o Cardioplegia o 2 return streams – pre and post aortic clamp
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What is off-pump coronary artery bypass grafting?
- This refers to a CABG on a beating heart without the use of cardiac bypass - An immobilisation device (octopus stabilisation system) is used to reduce movement of area of myocardium operating on CABG on a beating heart without the use of cardiac bypass.
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List vessels commonly harvested for use of CABG..
- Saphenous vein - Radial artery – in younger patients without calcified arteries - Internal mammary artery
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What are the advantages of off-pump CABG?
* Avoids complications of CPB * Earlier extubation * Reduced hospital/ITU stay
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What are the problems associated with off pump cardiac surgery?
- More technically demanding as moving heart – overcome partly by stabilisation device - Haemodynamic instability during handling of heart – lifted up and impairs LV filling / valves - Still risk of needing bypass – which may be more challenging when surgery already started
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Causes of haemodynamic instability in off pump CABG
- Reduced LV filling , contraction and CO o Heart lifted out of pericardial sac o Immobilised by octapus stabilisation system o Ischaemia - Arrhythmias and reduced CO o From handling the heart, ischaemia and reperfusion - Valve distortion and regurgitation - Bleeding
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What monitoring is required during off pump CABG
- Standard AABGI - Invasive arterial pressure monitoring - 12 lead ECG – conventional ECG is altered as heart is out chest. 12 lead is more accurate - TOE = to detect regional wall motion abnormalities (ischaemia) or air around the heart
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What are the anaesthetic goals during off pump CABG?
- MAP >70mmHG – using fluids, vasopressors or ionotropes - Maintain sinus = Treat arrhythmias / bradycardias – may need pacing wires / electrolyte Mx - Maintain temperature – hypothermia causes arrhythmias and coagulopathy - Good communication with surgeon e.g. TOE findings
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List the strategies that minimise haemodynamic instability ..
- Surgeon: o Minimise surgical manipulation and stop if major instability o Minimise periods of ischaemia by utilisation of shunts - Anaesthetist o Avoid electrolyte disturbances – keep K+ over 4.5 and give magnesium routinely o Keep HR low / normal – minimises O2 demand and hence reduces effects of ischaemia o Ensure patient is adequately filled guided by cardiac output monitoring
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List 2 methods that help minimise perioperative hypothermia during OPCABG
- Temperature measurement before and during case to target correctly - Increase ambient theatre temp - Warm IV fluids - Hot air warms – bair hugger - Foil hat - Minimise leaving patient uncovered
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What is the criteria for extubation after CABG surgery
- Patients optimised after a period on critical care o Weaned from respiratory support o Haemodynamically stable o Normal acid base / coagulopathy o No suspicion of bleeding
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What are the potential complications post-op following cardiac surgery?
- Bleeding - Arrhythmias - Tamponade - Pulmonary HTN - Neurological complications – cognitive dysfunction, stroke, ischaemic spinal cord - AKI
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List central neurological complications after CABG
- Post operative cognitive dysfunction o Subtle decline in cognitive function e.g. memory, concentration, executive function - Delirium o Acute, fluctuating disturbance in consciousness and attention. Shorter term than above - Stroke – hypoperfusion, embolic, haemorrhagic - TIA - Ischaemic spinal cord injury
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List peripheral neurological complications after CABG
- Brachial plexus = CVC, positioning, internal mammary artery havesting - Ulnar nerve = radial artery harvesting - Saphenous nerve = saphenous nerve harvesting - Phrenic nerve = internal mammary artery harvesting - Recurrent laryngeal = intubation , IMA harvesting
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Patient risk factors for development of neurological conditions post CABG
- Age - Pre op dementia - Pre-existing cerebrovascular disease e.g. hx of stroke , carotid stenosis - Diabetes, HTN
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List surgical risk factors for developing neurological complications post CABG
- Prolonged surgical time - Clamping diseased aorta and embolization - Use of CPB – clots from circuit, disruption to autoregulation in hypothermia / rewarming - Bleeding – poor cerebral perfusion pressure and O2 carrying capacity
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What are the anaesthetic factors that increase risk of developing neurological complications after CABG
- Hypotension – low MAP and inadequate CPP - Prolonged deep hypnotic state i.e. high level of burst suppression
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How can the risk of post op neurological complications be minimised during CABG
- Surgical o Minimally invasive – less stress response o USS To check for plaques before handling o Use bubble traps and filters when using CPB – remove air embolus and clots - Anaesthetic o Maintain MAP – arterial BP monitoring , vasopressors o Avoid excess anaesthesia – BIS o Normal physiological parameters – CO2, O2, electrolytes glucose o Use of cerebral oximetry o Avoid rapid rewarming – can result in cerebral oedema
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What are the special considerations when patients have had a CABG using left internal mammary artery graft over using vein graft?
- Prone to arterial spasm o Avoid NA o GTN may be helpful
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What is cardiac tamponade?
- Intrapericardial fluid build up – either serous fluid or blood - Resulting in ability of normal cardiac contraction - Obstructive shock
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Clinical features of cardiac tamponade What is Beck's triad?
- BECKS TRIAD – hypotension, muffled heart sounds, raised JVP - Increased vasopressor requirement - Tachycardia - Pericardial rub - If awake – breathless, chest pain
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What is pulsus paradox and Kussmaul sign – seen in spontaneous ventilating cardiac tamponade
- Pulsus paradox o >10mmHg drop in systolic BP during inspiration - Kussmaul sign o Rise / lack of fall of JVP with inspiration
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What are the causes of cardiac tamponade?
- CABG / cardiac surgery - Aortic dissection - Trauma - Iatrogenic damage to aorta during interventional cardiology procedure - Infectious pericarditis - Non infectious pericarditis – autoimmune, uraemia
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What are the ECHO findings in cardiac tamponade?
- Pericardial effusions - >20mm fluid around heart - Swinging heart sign – heart suspended in pericardium - Collapse of chambers - IVC dilation - Intraventricular septum left shift during spontaneous ventilation
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What are the CXR signs in cardiac tamponade
- Large globular heart - Evidence of HF / pulmonary oedema
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What are the ECG findings in cardiac tamponade
- Tachycardia - Low voltage QRS - Electrical alternans – beat to beat variation in QRS - Atrial arrhythmias
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What will be found on pulmonary artery catheterisation in cardiac tamponade
- Raised pulmonary artery wedge pressure
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How is cardiac tamponade managed?
- A to E = O2, avoid PPV where possible, vasopressors/ ionotropes / fluids - Diagnosis - Pericardiocentesis – now USS guided - Urgent cardiothoracic surgical review – thoracotomy / pericardiotomy?
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What are the surface landmarks for pericardiocentesis
- Apical o 1-2cm lateral to apex beat in 5th,6th or 7th intercostal space - Parasternal o Left parastenal edge 5th intercostal space 1cm lateral to sternum - Subxiphoid o Between xiphistenum and lower rib edge
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What are the complications of pericardiocentesis?
- Pneumothorax - Intercostal vessel damage - Laceration of coronary vessel / ventricle - Arrhythmias - Pneumopericardium - Pericardial depression syndrome – LV dysfunction and cardiogenic shock
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How to manage someone anaesthetically for surgical management of cardiac tamponade including haemodynamic goals
- If time – drain first - Otherwise – emergency decompressive sternotomy o Preparations – consultant anaesthetist / cardiothoracic surgeons , ECMO available, MHP activated o RSI with ketamine o Haemodynamic goals – full, fast and tight  Maintain SVR – MAP reliant on this and poor CO – coronary perfusion  Maintain preload  Maintain SR and avoid bradycardia – SV limited so CO dependant on rate  Maintain contractility – avoid excess cardiac depressants o Ventilatory strategies  Lowest possible pressures  Good FiO2  Avoid hypercarbia
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What is the specific risk post-op after cardiac tamponade correction?
- Re-expansion pulmonary oedema o During tamponade lungs may be partially collapsed due to pleural effusions, high thoracic pressures and reduced pulmonary perfusion o When decompressed sudden increase in venous return and abrupt re-expansion - Arrhythmias - Reoccurrence .
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What are the effects of IPPV during tamponade?
- Increased thoracic pressure - Initially causes compression of pulmonary vasculature and increase venous return to LEFT heart and increased SV - However also reduces venous return to right heart and reduced CO
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How is post cardiac surgery pulmonary artery hypertension managed?
- Avoid rise in pulmonary pressures – e.g. hypoxia, hypercarbia, acidosis - Pharmacological – inhaled nitric oxide / prostacyclin , IV sildenafil - Support cardiac function – IV milronone
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What are the most common causes of cardiac arrest following cardiac surgery?
* VF * Bleeding * Cardiac tamponade
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How does management of cardiac arrest differ following cardiac surgery?
- Same approach + work through reversible causes - If no reversible cause found and one cycle of external CPR / defib is unsuccessful then immediate chest re-sternomy o No time for skin prep – sterile gloves and gowns only o Internal cardiac massage and defibrillation
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What are the issues related to repeat cardiac surgery?
* Independent risk factor for perioperative mortality * Surgery is prolonged and complex due to adhesions * Increased risk of major blood loss * VF can occur on sternotomy/adhesiolysis * More likely in older patients with advanced comorbidities/poor physiological reserve
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What are indications for repeat sternotomy?
- Post CABG myocardial revascularisation – PCI first line but surgical revascularisation may be needed - Repeat valve surgery – mechanical valve , I.E or small annulus -i.e. transcatheter approach not possible.
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What are specific pre-op considerations for someone requiring repeat sternotomy?
- MDT planning – cardiac surgeon, anaesthetist, cardiologist, radiologist – risks, surgical approach - Surgical Hx – more challenging if within 3 weeks – 6months as adhesions more dense OR if previous radiotherapy - Risk scoring – e.g. Euroscore 2 - Imaging – CT / MRI to predict risk based on anatomy - Cross match and optimise anaemia - Patient counselling / risks discussed
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Describe the perioperative management in re-sternotomy surgery…
- AABGI + arterial line + TOE + CVC - CPB required? - Manage bleeding risk… o Good IV access o TXA – reduced transfusion need o Cell salvage o Reverse Trendelenburg to move heart away from sternum during sternotomy – decompresses heart o Ventilatory pause during sternotomy to move heart away from sternum o Prepare for CPB – preparation of cannulation site etc - Abx prophylaxis – risk of mediastinitis
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Why are re-sternomy patients at risk of major haemorrhage?
- Accidental injury of RV on re-sternotomy - Adhesions and prolonged dissection - Injury to great vessels on re-sternotomy
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What surgical method reduces bleeding on re-sternotomy
- Oscillating saw – cut under vision
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How is major hemorrhage during re-sternotomy managed?
- Apply direct pressure - If peripheral cannulas already in place, initiate full heparinisation and CPB and cardiotomy suction immediately - If no access – massive transfusion protocol activated and start CPB as soon as possible - Clotting factors – guided by ABG and ROTEM o Calcium o Fibrinogen / prothrombin complex
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What surgical closure strategies reduce injury/bleeding if re-sternotomy is required?
- CABGs should be routed away from the midline - Proximal CABG tagged with radiopaque marker to aid visualisation on angio - Safer sternal entry by covering heart and great vessels to reduce sternal adhesions - Possible to close pericardium but then risk of effusions and tamponade
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Post op care after re-sternotomy
- ITU care - Abx prophylaxis - Monitoring bloods / coagulopathy
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What is minimally invasive cardiac surgery?
- Procedures that avoid traditional midline sternotomy - May use endoscopes or smaller incisions o Mini sternotomy o Video assisted thoracoscopic surgery o Transcatheter methods
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What are examples of minimally invasive cardiac surgery?
* TAVI * Coronary angioplasty * Endoscopic thoracic sympathectomy * Minimally invasive CABG * Aortic valve replacement
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What are the benefits of minimally invasive cardiac surgery?
* Reduced post-op pain * Quicker recovery * Reduced bleeding * Reduced stress response * Better cosmetic appearance
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What are the risks of minimally invasive cardiac surgery?
* More technically difficult * May need to convert to sternotomy * No internal defib pads can be placed * Bleeding may not be apparent
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What classes of drugs might be taken by a patient who has had a heart transplant? plus side effects
- Immunosuppressant – calcineurin inhibitor – tacrolimus / cylosporin - Steroids – prednisolone - Other – azathioprine - Common regime = antimetabolite (azothiprine / mycophenolate mofetil) + calcineurin inhibitor + steroid Side effects of these - Common to all – increased infection, increased malignancy - Tacrolimus – renal toxicity , diabetes, arrhythmias - Myophenolate mofetil – bone marrow suppression - Ciclosporin – renal toxicity, HTN, diabetes , tremor - Azathioprine – bone marrow suppression
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How does the presence of a cardiac transplant alter anaesthetic pre-assessment?
- Aetiology of cardiac failure – systemic consequences? Congenital airway abnormalities - Graft function o ECHO , ECG , exercise tolerance - Medication related o Immunosuppression  Will need steroid replacement intra op  Risk of infection  Cyclosporin – hypertension  Steroids increase risk of diabetes  Tacrolimus – renal function o Seek advice from transplant team
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What adjustments are made perioperatively in those with heart transplant
- Avoid other nephrotoxic drugs – NSAIDS - Steroid cover - Strict asepsis and Abx cover due to increased infection risk - Good antiemetic cover to improve oral medication compliance - No use of atropine / glycol – use adrenaline for brady
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What atypical infections are associated with immunosuppression?
* Toxoplasmosis * Pneumocystis jirovecii * CMV * Candida albicans * Herpes simplex
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What physiological changes occur following a cardiac transplant?
- Donor sino atrial node has no innervation - HR 90-100 bpm – loss of vagal tone - Loss of normal vagal reflexes to peritoneal stretch / laryngoscopy / occulocardiac - No compensatory tachycardia with hypotension – loss of baroreceptor reflex - Exercise tachycardia response is blunted as entirely catecholamine driven. Similarly HR responses to postural changes are blunted - No pain in ischaemia / infarction
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How is pharmacological management altered in heart transplant patients?
- Atropine and glycopyrrolate have no effect - Sux and neostigmine have no bradycardic effects - Upregulation of receptors on donor heart means adenosine and adrenaline have an increased effect
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Intra op management in patient with heart transplant having another surgery
- Steroid cover - Invasive monitoring – TOE / arterial line - Strict asepsis - Removal lines as soon as possible - Abx cover - Adequate pre load
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What are comorbidities that a patient with a heart transplant may have?
- CVS o Cardiac allograft vasculopathy – immunological and non-immunological cause of atherosclerosis of donor coronary arteries o Rejection causing reduction in graft function o HTN and diabetes from immunospressive meds - other o Epilepsy and reduced seizure threshold with tacrolimus and ciclosporin o Ongoing consequences of original disease that required transplant e.g. sarcoid / amyloid
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What investigations are required to assess function of transplanted heart prior to unrelated surgery?
- ECG – resting HR and rhythm - ECHO – valve/ EF - CXR – pulmonary oedema/ HF - CT angiography - Functional test – CPET
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What is orthotopic heart transplant?
Donor heart is placed in the same position as the old heart.
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What are core technical advantages of 3D-TOE over 2D-TOE?
* Volumetric imaging * Quantitative analysis: accurate measurements of volumes, areas, and distances without geometric assumptions. * Enhanced spatial orientation: visualization of complex anatomy aiding in surgical planning * Improved assessment / visualisation of prosthetic valves and devices
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What are three limitations of 3D-TOE in the perioperative setting?
* Lower temporal resolution: Compared to 2D imaging, which may affect the assessment of rapidly moving structures. * Potential for artifacts: especially in arrhythmias * Requires more processing power and storage capacity. * Demands additional training for interpretation
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What are uses of 3D TOE?
- Valve assessment – MR evaluation, AS severity or regurgitation jets quantification - Heart structure and function o Left atrial appendage o LV function and regional wall motion o abnormalities o RV size / function – aid diagnosis of PAH o CHD where anatomy is complex - Thoracic aorta aneurysm / dissection / atheroma - Perioperative planning and monitoring o Guidance for left atrial appendage closure or MR correction o Assists in transeptal puncture o Haemodynamic assessment – CO monitoring - Education – 3D models can be made for surgical planning and education
362
How does 3D-TOE enhance evaluation of mitral regurgitation?
- Enface visualisation – provides precise surgical view of mitral valve - Quantitative assessment – regurgitant jet measurement using 3D colour doppler - Mechanism identification – assesses MR leaflet motion and annular geometry to differentiate between degenerative or function MR - Guides intervention o Pre op planning and surgical approach o Intra op monitoring for successful repair and assessing stenosis o Post op assessment
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How is 3D TOE used in assessment of left atrial appendage?
- Thrombus detection – e.g. before cardioversion - Morphology evaluation – e.g. LAA size / shape – for device sizing in occlusion proceedure - Device deployment guidance – aids positioning and confirm device placement for LAA closure
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How does 3D TOE assist in transeptal puncture in percutaneous interventions
- Anatomical visualisation – real time imaging of intra-atrial septum and surrounding structures - Hence puncture site selection for optimal location to minimise complciations - Needling guidance – direct real time imaging of needle through septum
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What are benefits of using 3D TOE for LV/RV volume and function assessment?
- Accurate volume measurement and hence EF calculation more accurate - Enhanced detection of regional wall motion abnormalities - Hence improved diagnosis of PAH through shape and size of RV
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How is 3D TOE used in evaluating tricuspid valve pathology?
- Leaflet assessment – better visualisation of all 3 leaflets – identifies prolapse, perforation etc - Annular measurement – assesses dilation - Regurgitation jet quantification
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What advantages does 3D-TOE offer in aortic valve assessment?
* Improved visualisation and anatomical detail * Enhanced assessment of stenosis severity
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How does 3D-TOE contribute to the assessment of the thoracic aorta?
* Diagnosis of Aneurysm, dissection, atheroma including if theres an embolization risk .
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What can near infrared spectroscopy be used for?
- Cerebral oxygenation measurements - Used during surgery e.g. cardiac surgery or carotid endartectomy or high risk pts
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How does near infrared spectroscopy work for cerebral oxygenation measurements
- Sensors applied to forehead and light emitted at 760nm and 850nm – near infrared range - Absorbed by oxy and deoxy Hb and scattered back and detected by sensor - The ratios are compared to determine the % saturations - Relies on beer and lamberts law
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What is aortic dissection?
Tear in intima allows blood to flow between intima and media creating false lumen.
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How is aortic dissection classified?
- Stanford o Type A – ascending aorta +/- arch o Type B – descending aorta only - DeBakey o Type 1 - ascending aorta + arch + descending o Type 2 – ascending only o Type 3 – descending only
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What are risk factors for aortic dissection?
* Hypertension * Marfan syndrome * Ehlers-Danlos syndrome * Trauma * Iatrogenic causes
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How does aortic dissection present?
- Chest pain radiating to back severe, sudden onset, ripping - Aortic diastolic murmur - Shock - Systolic BP/ pulse deficit difference in limbs - Focal neuro deficit
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How is aortic dissection diagnosed?
CT angiogram is the gold standard; ECHO can also be used.
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How is aortic dissection managed?
- A to E - Depends on type o Type A – surgical emergency o Type B – medical management - Analgesia – reduces sympathetic surge / myocardial stress - BP – reduce BP and HR o aim systolic 100-120mmHg , HR < 60bpm - prepare for major haemorrhage - Cardiothoracic referral
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Complications of aortic dissection
- Tamponade - Stroke - MI - Renal failure - Spinal ischaemia
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What are common vasopressors used in management?
* Noradrenaline * Adrenaline * Vasopressin * Methyl blue
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dose, action and risks of adrenaline and noradreanline
Noradrenaline - 0.05-0.1 ug/kg /min - A1 receptors to increase arterial and venous tone - Risks – tachyarrhythmias, MI, AKI Adrenaline - 0.01-0.05 mcg/kg/min - Alpha and beta agonist – more Beta activity than NA - Strong ionotrope too - However – tachyarrhythmias, hyperglycaemia, lactic acidosis, hypokalaemia (B2 effect)
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dose , action and risk of vasopressin
Vasopressin - 0.02 – 0.04 units / min - V1 receptor agonist – non catecholamine – reduces NA requirements - Lower risk of tachyarrhythmias and preserves renal function - However risk of digital ischaemia , hyponatraemia , worst for splanchnic vasoconstriction
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mechanism and side effects / contraindicaition of methyl blue
Methyl blue - Inhibits nitric oxide synthase and guanylate cyclase – reduces vasodilation - Side effects – green urine, pulse ox unreliable - Contraindicated in glucose 6P dehydrogenase deficiency – methaglobinaemia and haemolysis
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What key risk factors increase perioperative morbidity following cardiac surgery?
* Previous ACS * CCF * Hypertension * Previous cardiac surgery * Aortic atheroma - CKD, COPD, neurological disease
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What is the Duke Activity Status Index questionnaire?
- 12 questions related to activities of daily living - Allows estimation of metabolic equivalent of tasks - < 4 METS = risk of adverse outcome
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What scoring systems assess risk in cardiac surgery?
- EuroSCORE o Patient related factors = > 60yrs, female, COPD, CKD, previous cerebrovascular disease, active endocarditis, previous cardiac surgery o Cardiac related factors = recent MI, unstable angina, PAH, LV dysfunction o Operation related = emergency, operation other than isolated CABG - Parsonett factors o Patient = age, sex, obsesity, diabetes, HTN , CKD o Cardiac – intra aortic balloon pump required , LV dysfunction o Surgical = mitral or aortic valve , valve plus CABG - Both predict mortality
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What factors increase the risk of perioperative arrhythmias?
- Patient factors: o Electrolyte imbalance  hypokalaemia (depresses automaticity, AV block, causes early depolarisations  hyperkalaemia – conduction delays, VF / VT  hypocalcaemia – prolongs AP, risk of torsades o Myocardial ischaemia – early depolarisations, re entry o Increased sympathetic activity – sepsis , hypoxia, acidosis, stress of surgery o Vagal stimulation – severe bradycardia - Pharmacological factors: o IV anaesthetic agents  Most depress sympathetic activity – bradycardias  Ketamine – increases sympathetic activity and prolongs QT o Opioids  Bradycardias  Methadone – increases QTc o Neostigmine  Bradycardia and AV block o Vasopressors  Reflex bradycardia - Surgical factors o Cardiac or thoracic surgery
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What is the typical management for most perioperative arrhythmias?
* majority do not require treatment and self resolve * treatment includes o treating underlying cause o haemodynamic support o cardioversion – electrical or with antiarrhythmic drugs * Pre operative assessment o ECG for all patients with CVS disease – detect ischaemia, infarct, hypertrophy, long QTc, BBB, arrhythmias o ECHO o Cardiology consultant may be needed o Surgery delayed if trifascicular block, advanced heart block, new onset LBBB, SVT o Indications of antiarrhythmics  Symptom relief  Improving cardiac function  Preventing life threatening arrhythmias * Intra op o If arrhythmia develops, try treat the cause, o Evaluate cardiac function o Choose antiarrhymic carefull  Avoid b blockers in asthma  Avoid amiodarone in severe lung disease  Avoid CaCB in acute HF * Post op o May require continuous cardiac monitoring / ICU admission if unstable prevention - risk factors for arrhythmias should be corrected pre op ## Footnote Most arrhythmias are transient and do not need intervention.
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What is the first-line management for perioperative AF?
- First line – esmolol / B blocker - For impaired ventricular function – Digoxin + B blocker/ CaCB - For cardioversion without electrical – amiodarone ## Footnote These medications help control heart rate in AF.
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dose of adenosine, amiodarone, atropine, digoxin, metoprolol
adenosine = 6mg, 6mg, 12mg amiodarone = 300mg bolus over 10 mins, 900mg over 23hr atropine = 600mcg - up to 3mg digoxin = 0.25 to 0.5mg bolus metoprolol = 1-5mg
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What pharmacological methods can manage broad complex tachycardia
- Amiodarone 300mg loading and then 900mg over 24 hours or lidocaine -torsades = MgSO4