Periop cardiology Flashcards

1
Q

What is the aeitology of aortic stenosis?

A

Acquired: Calcification (degnerative), rheumatic
Congenital: bicuspid, unicuspid, quadricuspid

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2
Q

What is the presentation of aortic stenosis?

A
  • Angina
  • Syncope
  • Dyspnoea
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3
Q

What is the severity grading of Aortic stenosis?

A

Normal: Valve area > 2cm2, Vmax <2 m/s
Mild: Mean gradient <20mmHg, valve area 1.5-2cm2, Vmax 2-2.9
Mod: Mean gradient 20 - 40mmHg, valve area 1-1.5, Vmax 3 - 3.9
Severe: Mean gradient >40mmHg, valve area <1, Vmax >4

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4
Q

What is the management of aortic stenosis?

A
  • Antihypertensives
  • Balloon valvloplasty
  • TAVI
  • Open AV replacement
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5
Q

What are the anaesthetic goals for a patient with aortic stenosis?

A

“Slow, full and tight “

  • rate = low normal
  • rhythm = maintain sinus rhythm is critical (atrial kick may contribute up to 40%of preload)
  • preload = careful balance, keep filled but also prone to pulmonary oedema
  • afterload = critical to defend MAP for adequate coronary perfusion
  • contractility = maintain
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5
Q

What is the aetiology of aortic regurgitation?

A

Acute: Infective endocarditis, aortic dissection
Chronic: Rheumatic, connective tissue eg Marfan, elhers-danlos, arthritic disease eg Ank spond, RA, SLE

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5
Q

What is the presentation of Aortic regurg?

A

Acute: Sudden LV volume overload -> CCF
Chronic: Gradual LV dilation -> LV Dysfunction
- widened pulse pressure, collapsing pulse (waterhammer)

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5
Q

How is aortic regurg severity rated?

A

Jet width (%LVOT)
Normal and mild < 25
Moderate 25-65
Severe >65

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5
Q

What is the treatment for aortic regurg?

A

-Aortic valve replacement
- Antihypertensives for chronic AR

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6
Q

What are the anaesthetic goals for managing aortic regurgitation?

A
  • Rate: High/normal
  • Rhythm: Sinus rhythm (less critical)
  • Contractility: Maintain
  • Preload: Keep filled
  • Afterload: Reduced

-For hypertension use arteriolar vasodilator (phentolamine) > venodilator (GTN)

  • For hypotension ephedrine > metaraminol
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7
Q

What is the aetiology of mitral stenosis?

A

Use acquired via rheumatic heart disease

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8
Q

What is the presentation of mitral stenosis?

A
  • Angina
  • Dyspnoea
  • Syncope
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9
Q

How do you grade the severity of mitral stenosis?

A

Valve area in cm2 (although HR and filling are major determinents)

Normal 4 -6
Progressive 1.5 - 4
Asymptomatic severe < 1.5
Symptomatic severe <1

Progressively get worse pulmonary hypertension and LA dilation

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10
Q

What are the treatments for mitral stenosis?

A
  • Anticoagulation if in AF
  • Rate control
  • Percutaneous balloon valvuloplasty
  • Mitral valve surgery
  • Excision of LAA if recurrent embolic events
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11
Q

What are the anaesthetic goals for mitral stenosis?

A

Rate: Slow/normal (tachycardia bad)
Rhythm: Critical to maintain SR if in sinus (early Cardioversion)
Contractility: Normal (RV may be reduced due to pulm HTN)
Preload: Maintain normal
Afterload: Maintain

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12
Q

What is the aeitology of mitral regurg?

A

Acute: ruptured chordae tendinae, infective endocarditis
Chronic: LV dilation, connective tissue, rheumatic heart disease

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13
Q

What is the presentation of mitral regurg?

A

Acute: APO
Chronic: AF

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14
Q

What is the grading severity of mitral regurg?

A

Progressive <50% regurg, central jet 20-40%
Severe >50% regurg, central jet >40%

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15
Q

What is the treatment for mitral regurg?

A

Primary MR -> mitral valve repair rather than replacement

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16
Q

What are the anaesthetic goals for mitral regurg?

A

Heart rate: High/normal
Rhythm: Sinus
Contractility: Normal
Preload: Low/normal
Afterload: Low/normal (promote forward flow)

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17
Q

What is the aetiology of HOCM?

A

-asymmetrical hypertrophy of the septum (usually anterior) causing dynamic obstruction of the LVOT

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18
Q

What is the presentation of HOCM?

A
  • Exertional angina/dyspnoea
  • LVH on ECG and deep sharp Q waves inferiolateral
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19
Q

What is the management of HOCM?

A
  • Beta blockers, ca channel blockers
    -AICD and pacemaker
  • Myomectomy
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20
Q

What are the anaesthetic goals with HOCM?

A

Heart rate: low/normal
Rhythm: Sinus (critical)
Contractility: Normal (Avoid increases eg inotropes)
Preload: Keep full
Afterload: High/normal (splints LVOT)

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21
Q

What is the definition of heart failure?

A

failure of heart to meet oxygen
demands of body resulting in tissue hypoxia and end-organ damage

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22
Q

What are the classifications of heart failure?

A

-HFrEF (HF with reduced EF <40%) (i.e Systolic dysfunction)
-HFpEF (HT with preserved EF >50%) (ie. Diastolic dysfunction)
- HFmrEF (HF with mid-range EF 40-49%) i.e also diastolic dysfunction

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23
Q

What is the diagnosis of HFpEF?

A

Hard to diagnose
- TTE: evidence of impaired filling, non-dilated LV, LVH, increased LA vol.
- PCWP: >15mmHg
- LVEDP: >16mmHg

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24
Q

What is the treatment of HFpEF?

A
  • Nil evidence for effective mx
  • Mainly aim to treat co-morbidities eg resp disease, obesity
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25
Q

What is the diagnosis of HFrEF?

A
  • LV EF <40% on TTE
26
Q

Which HF are high risk and what is their physiology?

A

severe HF (EF<30%) are very high risk, depend on preload for V filling
and rely on increased SNS tone.

Should only undergo absolutely necessary surgery

27
Q

What are the pre-op considerations for a patient with heart failure?

A

Medication management: Continue anti-failure thearpies eg beta blockers, Ace inhibitors, statins, diuretics

?AICD: if insitu will need to be deactivated, and revert PPM to backup mode

ECG and TTE preop to risk stratify

28
Q

What are the intra-operative goals for a patient with heart failure?

A
  • minimize negative inotropy, tachycardia, diastolic hypotension and systolic hypertension.
  • Defend renal perfusion.
  • Consider regional if possible
29
Q

What are some post operative considerations for patients with heart failure?

A
  • Disposition eg HDU/ICU
  • Adequate analgesia (reduce tachycardia due to pain)
  • Restart anti-failure meds as soon as possible
30
Q

What is the guideline for patients undergoing surgery with recent MI?

A

Delay >60 days unless emergency surgery that cannot wait

31
Q

How do you Quantify perioperative cardiac risk?

A
  • use a validated risk-prediction tool (e.g. RCRI or ACS surgical risk calculator)
  • if low risk (Major Adverse Cardiac Event < 1%) then proceed
  • if high risk (MACE ≥ 1%) then estimate exercise tolerance
  • If METS > 4 then proceed, if METS < 4 then stress testing (if will change management)
32
Q

When do you and don’t you stress test patients?

A
  • If negative stress test, CT-CA within the last year then don’t repeat stress testing
  • If had intervention in the last year and no new sx then don’t stress test eg PCI
  • If negative stress test then good NPV and can proceed confidently
  • If positive, poor PPV so will need cardiology opinion
33
Q

What are the indications for revascularisation?

A
  • symptomatic CAD
  • asymptomatic CAD with:
  • LM ≥ 50%
  • LAD ≥ 70% with positive stress test
  • ≥ 70% in 3 major vessels
  • ≥ 70% in 2 major vessels + positive stress test
34
Q

How long should you wait for surgery after BMS, DES, CABG?

A

BMS: 30 days
DES: ideally at least 6 months, not less than 3 months
CABG: 4 - 6 weeks

35
Q

What is the definition of pulmonary hypertension?

A

mPAP >20 mmHg at rest on right heart cath

36
Q

What are the 5 types of pulmonary hypertension?

A

1: Pulmonary arterial hypertension
2: PH secondary to left heart disease
3: PH secondary to lung disease
4: PH secondary to chronic VTE
5: Unclear multifactorial

37
Q

How do you assess severity of Pulmonary hypertension?

A

Hx:
- medications
- symptoms of RH failure
- Symptoms of low cardiac output eg syncope/angina
- Functional capacity

Exam:
- signs of RH failure eg peripheral oedema, raised JVP, pulsatile liver, parasternal heave
- 6 minute walk test (600 m is ok, <300m is high risk)

Ix:
- Vitals eg hypoxia
- TTE: RVSP, LVEF, RV function eg TAPSE
- Right heart cath:
Mild 20-40
Mod 40-55
Severe >55

38
Q

What are the pre-operative considerations for a patient with pulmonary hypertension?

A
  • Cardiac optimisation (in consultation with cardiologist)
  • Optomise pulmonary vascular resistance (pulmonary dilators)
  • Optomise preload (diuretics)
  • Optomise cardiac function (inotropes)
39
Q

What are the intra-operative considerations for a patient with pulmonary hypertension?

A
  • Regional vs GA
  • Adequate monitoring
  • Avoid factors that increase Pulm vasc resistance:
  • SNS surge (pain, laryngoscopy)
  • Acidosis
  • Hypercapnia
  • Hypoxaemia
  • Hypothermia
  • High PEEP
  • Drugs eg N20 and ketamine
  • Normal Tidal volumes and ventilator pressures to keep normal lung volumes
  • Avoid sudden drop in SVR (decreased coronary perfusion and increased myocardial ischaemia)
  • Have rescue drugs that can decrease pulmonary vasc resistance eg NO, Prostacyclin
40
Q

What are the post operative considerations for patients with pulmonary hypertension?

A
  • Disposition
  • Appropriate monitoring
41
Q

What is pulmonary hypertensive crisis?

A
  • acute on chronic increase in pulm vasc resistance
  • due to acute increase in vascular tone of pulm vasculature
42
Q

What is the pathophysiology of pulmonary hypertensive crisis?

A
  • Rapid increase in Pulm vasc resistance
  • Increase in RV afterload
  • Increase in RV pressure which reduces LV preload and coronary perfusion
  • Leads to myocardial ischaemia and subsequent hypoxia and acidosis which then worsens the pulm vasc resistance
43
Q

What are clinical signs of pulmonary hypertensive crisis?

A
  • Hypoxia
  • Hypotension
  • Decreased etCO2
  • Sinus tachycardia
  • Elevated CVP
44
Q

What is the treatment of pulmonary hypertensive crisis?

A
  • 100% O2 (vasodilator)
  • Hyperventilate (decrease CO2)
  • Decrease airway pressures
  • Correct acidosis
  • Administer pulmonary vasodilators
  • Support cardiac output i.e inotropes such as adrenaline
  • Analgesia (if pain causing crisis)
  • ECMO
45
Q

What are some of the physiological differences between a normal heart and a heart transplant?

A
  • Transplant has no sensory, parasympathetic or sympathetic innervation
  • Resting HR is ~90-110 in heart transplant
  • CO in transplant is very preload dependent
46
Q

What are some of the differences in pharmacological responses in heart transplants?

A
  • Nil response to atropine/glyco
  • Increased response to adrenaline and noradrenaline
47
Q

What are some pre op considerations for a patient with heart transplant?

A
  • What was indication for tranplant, ?systemic disease
  • Any signs of recent rejection
  • Current cardiac function (coronary artery disease is common and doesn’t present with angina) eg functional status, recent TTE, angiogram
  • Transplant meds -> continue during periop period, any side effects eg renal impairment
48
Q

What are some intra op considerations for a patient with heart transplant?

A
  • Strict asepsis, with all lines and medications
  • Careful positioning due to skin related steroid changes
  • consider stress dosing steroids
  • Maintain preload and cardiac output
  • Maintain SVR and afterload from coronary perfusion
  • Maintain MAP
  • judicious dosing of adrenaline/noradrenaline
49
Q

What are some post op considerations for a patient with heart transplant?

A
  • Restarting immunosuppression
  • Disposition
  • Early removal of lines
  • Discussion with ID regarding ongoing ABx
  • Careful fluid monitoring to avoid overload/dry
  • Monitor renal function
50
Q

What are the causes of QT prolongation?

A
  • Electrolytes eg, Hypokalaemia, Hypomagnesaemia, Hypocalcaemia
  • Hypothermia
  • Medications/drugs

Less common:
- Myocardial ischemia
-ROSC Post-cardiac arrest
-Raised intracranial pressure
-Congenital long QT syndrome

51
Q

What is the risk of QT prolongation?

A

Can become torsades de point and degnerate into VF
- treated with 2g Mg

52
Q

What drugs prolong QT?

A
  • Ondansetron, droperidol
  • Amiodarone
  • Methadone
  • Erythromycin/azithromycin
  • Sux
  • Atropine/glyco
53
Q

How do you calculate QTc?

A

QTc = QT/square root of RR, where RR = 60/HR

54
Q

What is a normal QT?

A

Men < 440ms
Women < 460ms
>500 is concerning for torsades

55
Q

What are the anaesthetic issues with prolonged QT?

A
  • Minimise stress (triggers arrythmias): anxiolysis, analgesia
  • Avoid hypothermia
  • Maintain normal electrolytes
  • Avoid meds that prolong QT
  • Reversal may prolong QT so use atracurium/cisat that don’t need reversal
56
Q

What are causes of a systolic murmur?

A
  • Flow mumur (usually young people)
  • Aortic stenosis
  • Aortic sclerosis
  • Mitral regurg
  • HOCM
57
Q

Whats eisenmenger syndrome?

A
  • Severe pulm HTN due to left to right shunt (and pulm vol overload)
  • If pulm BP > sys BP can cause reversal of this shunt and systemic hypoxia
58
Q

What are the key anaesthetic goals in a patient with eisenmenger syndrome?

A
  • Maintain Systemic pressure (SVR)
  • Minimise pulm vasc resistance
    (to ensure its above pulm pressure and you don’t reverse the shunt)
59
Q

What factors increase pulm vasc resistance?

A
  • Catecholamines
  • Hypoxia
  • Hypercarbia
  • Hypothermia
  • High lung volumes
  • Acidosis
60
Q

What is the physiology behind a post fontan repair patient?

A
  • Blood flow to and through the lungs is passive
  • Needs high CVP, low PVR and low LA and LV diastolic pressures
61
Q

What is important in managing post fontan repair patient?

A
  • SR is critical, do not tolerate arrythmias
  • Tolerate hypovolaemia poorly
  • Are preload dependent
  • Low Pulm vasc resistance
62
Q

What are significant TTE finds on a patient with severe Aortic stensois?

A
  • Qualititative: calcified leaflets with reduced mobility, LV hypertrophy, Raised LAP, post stenotic aortic dilation, +/- late changes RV/LV
  • Quantitiative: valve area <1cm2, transvavlular gradient >40 amd Vmax >4m/s and diastolic dysfunction
63
Q

What are the types of cardiomyopathy?

A
  • Dilated
  • hypertrophic
  • Restrictive
  • Arrhythmogenic right ventricular
  • Unclassified
64
Q

What are the causes of dilated cardiomyopathy?

A
  • Idiopathic
  • Toxins eg alcholol, drugs
  • Post viral
  • Post partum
  • Duchenne’s muscular dystrophy
65
Q

What are the anaesthetic implications of dilated cardiomyopathy?

A
  • Rate: Normal
  • Rhythm: maintain sinus
  • Preload: Maintain
  • Afterload: Maintain
  • Contractility: Avoid myocardial depression, often require dobutamine/PDE inhibitors eg milrinone
66
Q

What are the causes of restrictive cardiomyopathy?

A
  • amyloid myocardial infiltration most common
  • other rare causes (idiopathic, endomyocardial fibrosis)
67
Q

What is the anaesthetic management of restrictive cardiomyopathy?

A
  • very challening
  • avoid peripheral vasodilation, decreased preload or decreased inotropy
  • Spont vent is preferred to maintain Venus return
  • ketamine is a useful induction drug
  • Rate: Normal
  • Rhythm: Sinus
  • Preload: normal/high
  • Afterload: High/normal
  • Contractility: Avoid negative inotropes