Cardiac surgery and interventional cardiology Flashcards
An adult patient undergoing cardiac surgery exhibits excessive bleeding following
cardiopulmonary bypass. A thromboelastogram performed on their blood is shown
below. The most likely cause of the bleeding is
(ROTEM with low Extem A10 and normal Fibtem A10)
a) Platelets
b)Fibrinogen
c) FFP
d) TXA
Plateltes
Fibrinogen if low Fibtem
TXA if curves tail off early
FFP if MCF low
A transjugular intrahepatic portosystemic shunt procedure is contraindicated in
patients with:
a) Hepatorenal syndrome
b) Refractory ascites
c) Severe TR
d) Variceal bleeding
e) Budd chiari
c) Severe tricuspid regurgitation (TR)
Severe TR can lead to increased right atrial pressure, which may impede the proper function of the TIPS and worsen outcomes.
Contraindications:
Severe Hepatic encephalopathy
Severe Pulmonary Htn
Severe TR
Multiple Hepatic Cysts
Coagulopathy (relative contraindication)
The image below shows the arterial pressure (red, upper line) and balloon pressure
(blue, lower line) from an intra-aortic balloon pump set at 1:2 augmentation. The
point of the waveform indicated by the large green arrow is called:
a) Assisted end diastolic
b) Assisted systolic
c) Unassisted end diastolic
d) Assisted systolic
Assisted end diastolic
Organ procurement after circulatory death is generally stood down if the time from
cessation of cardiorespiratory support to circulatory death extends beyond:
a) 60min
b) 90min
c) 120min
90 mins
30mins
Liver
Pancreas
Heart
60mins
Kidneys
90mins
Lungs
Page 35 ANZICS statement 2.4.3 Warm ischemia time
Donate life
The bipolar leads of a 12-lead electrocardiogram are:
a) All
b) V1-V6
c) aVL, aVR, aVF
d) I, II, III
e) None
D) I, II, III
3-electrode system
- Uses 3 electrodes (RA, LA and LL)
- Monitor displays the bipolar leads (I, II and III)
Life in the Fast Lane
The time for reversal of therapeutic dabigatran after administration of
idarucizumab 5 g is:
a) 5 mins
b) 15 mins
c) 30 mins
d) 60 mins
e) 120 mins
5 mins
- Essentially one circulation time
Intravenously administer the dose of 5 g (2 vials, each contains 2.5 g) as
o Two consecutive infusions or
o Bolus injection by injecting both vials consecutively one after another via syringe
Idarucizumab was administered as one 5 g intravenous infusion over five minutes
Among the 90 patients with available data, the median maximum reversal of the pharmacodynamic anticoagulant effect of dabigatran as measured by ECT or dTT in the first 4 hours after administration of 5 g idarucizumab was 100%, with most patients (>89%) achieving complete reversal. Reversal of the pharmacodynamics effects was evident immediately after administration.
FDA Product Guide
See blue book article
Interference with pacemaker function can result from all of the following EXCEPT:
a) RF ablation
b) High volume ventilation
c) Peripheral nerve stimulator
d) CT
e) Diathermy
d) CT
British Heart Rhythm Societies guidelines
When auscultating the heart the Valsalva manoeuvre will increase the murmur
intensity of:
a) AS
b) MS
c) MR
d) MVP
e) VSD
Mitral valve prolapse
Valsalva increases the strength of murmurs due to hypertrophic obstructive cardiomyopathy and mitral valve prolapse. It decreases the intensity of aortic stenosis, mitral stenosis, aortic regurgitation, mitral regurgitation, and ventricular septal defects.
OPPOSITE IS TRUE FOR SQUATTING (Increases preload)
A patient with a perioperative troponin rise above normal, chest pain, left ventricular
anterior regional wall motion abnormality, and atheroma without thrombus
occluding 70% of the left anterior descending coronary artery has had a/an
NSTEMI
STEMI
Unstable angina
Acute myocardial injury
Chronic myocardial injury
Type 1 MI
Type 2 MI
NSTEMI
MINS: MI/ischemic myocardial injury that doesn’t fulfill MI defn
MI: Myocardial injury with rise/fall cTn above 99th percentile of upper ref limit within 30 days post op plus at least one of:
Ischemic symptoms
New ischemic ECG changes
New path Q waves on ECG
Imaging evidence of myocardial ischemia
Angiographic/autopsy evidence of coronary thrombus
NP A medication that has NOT been associated with arrhythmogenic potential in patients with Brugada syndrome is:
a) Propofol
b) Thiopentone
c) Amiodarone
d) Ketamine
MAYANK B Thiopentone
BJA article 2018
Propofol infusions have been associated with a brugada like ECG.
The abnormalities seen in the electrocardiogram below are consistent with:
a) Hypercalcaemia
b) Hypermagnasaemia
c) Hyperphosphataemia
d) Hypokalaemia
e) Hyperkalaemia
NAOMI
ECG features of hypokalemia:
Increased P wave amplitude
Prolongation of PR interval
Widespread ST depression and T wave flattening/inversion
Prominent U waves (best seen in the precordial leads V2-V3)
Apparent long QT interval due to fusion of T and U waves (= long QU interval)
You are anaesthetising an 18-year-old who has a Fontan circulation for exploratory laparotomy. They are intubated and ventilated with a ventilator that has been brought from the Intensive Care Unit. Their current arterial oxygen saturation is 70%. To improve oxygenation, you should INCREASE the:
a) Increase PIP
b) Increase PEEP
c) Increase inspiratory time
d) Increase expiratory time
D) increase expiratory time
Reworded repeat, but prev options don’t directly align with these
Answer from then
Patients who have undergone the Fontan procedure depend on blood flow through the pulmonary circulation without the assistance of the right ventricle. The difference between central venous pressure and systemic ventricular end-diastolic pressure (termed the “transpulmonary gradient”) is the primary force promoting pulmonary blood flow and, more importantly, cardiac output.
Circulation in the Fontan patient is promoted by low pulmonary vascular resistance. Positive-pressure ventilation with increased tidal volumes, as described above, can result in excessive intrathoracic pressures, leading to decreased venous return to the heart and increased pulmonary vascular resistance.
In periods of low oxygen saturation, 100% inspiratory oxygen is appropriate.
The addition of PEEP will increase intrathoracic pressure, reducing venous return.
Trendelenberg positioning would increase CVP and therefore bloodflow through pulmonary circulation.
BJA: fontan circulation:
For relatively short procedures, Fontan patients are probably better off breathing spontaneously, as long as severe hypercarbia is avoided. For major surgery, or when prolonged anaesthesia is required, control of ventilation and active prevention of atelectasis is usually advisable. Potential disadvantages of mechanical ventilation in Fontan patients relate to the inevitable increase in mean intrathoracic pressure. This causes decreased venous return, decreased pulmonary blood flow, and hence, decreased cardiac output. Low respiratory rates, short inspiratory times, low PEEP, and tidal volumes of 5–6 ml kg−1 usually allow adequate pulmonary blood flow, normocarbia, and a low PVR. Hyperventilation tends to impair pulmonary blood flow, despite the induced respiratory alkalosis, because of the increased mean intrathoracic pressure.
https://academic.oup.com/bjaed/article/8/1/26/277637
You are called to assist with a patient in the intensive care unit who has had cardiac surgery three days ago and is now in cardiac arrest. External cardiac massage should aim for a systolic blood pressure of
a. 40
b. 60
c. 80
d. 100
e. 120
REPEAT
b. 60
BJA Article - Management of cardiac arrest following cardiac surgery - BJA Education
In the CICU, the effectiveness of ECC is confirmed by monitoring the arterial pressure trace with a target compression rate and depth to achieve a systolic impulse of > 60 mm Hg to maintain a mean perfusion pressure, preventing ventricular distension, LV wall stress, and ischaemia.
A 65-year-old man is undergoing coronary artery bypass grafting. Immediately upon commencing cardiopulmonary bypass and prior to administering cardioplegia, the aortic line blood appears the same colour as the blood in the venous cannulae, and the low venous saturation alarm is activated on the bypass machine. The most appropriate management at this point is to:
a) Attach another oxygen tubing to oxygenator
b) Increase the oxygen mix with air:oxygen blender
c) Ventilate and wean bypass
alternative remembered answers:
- Ventillate with 100% and continue
- Give O2 via side line
- Wean from bypass and ventilate lungs
- Inc blender FiO2
*Failure of oxygenation
I think wean bypass and ventilate - thoughts?
During rewarming on cardiopulmonary bypass, the most reliable surrogate for cerebral temperature measurement is:
A) Nasopharynx
B) Oxygenator arterial outlet
C) Oxygenator venous inflow
D) Bladder temp
E) PA Cath
A) Nasopharyngeal
Proximity to brain
Consistent correlation with core and brain temperature changes
Accessibility
Oxygenator blood temp represents temp of blood leaving circuit and doesnt reflect blood perfusing the brain
Clinical Techniques in Cardiovascular and Thoracic Surgery: This textbook discusses the monitoring of cerebral temperature during CPB and often cites nasopharyngeal temperature as a standard method due to its proximity to the brain.
Reference: Sabik, Joseph F., et al. “Temperature management and monitoring during cardiopulmonary bypass.” In: Clinical Techniques in Cardiovascular and Thoracic Surgery, edited by Little Brown and Company, 1998.
Perfusion: This journal article discusses various techniques for monitoring cerebral temperature during CPB, emphasizing the use of nasopharyngeal temperature probes.
Reference: Zollinger, Andreas, et al. “Temperature Management and Monitoring During Cardiopulmonary Bypass.” Perfusion, vol. 18, no. 1, 2003, pp. 3-9. doi:10.1191/0267659103pf582oa.
The image below is from the transoesophageal echocardiogram of an adult patient who is about to undergo cardiac surgery. The structure labelled with the arrow is the:
TOE image - four chamber, with arrow pointing to leaflet closest to septum
A) Anterior mitral leaflet
B) Posterior mitral leaflet
C) Tricuspid septal leaflet
D) Tricuspud anterior leaflet
E) Tricuspid posterior leaflet
A) Anterior mitral leaflet
A 45-year-old received a heart transplant one month ago. They develop a new supraventricular tachyarrhythmia without hypotension during gastroscopy. The most appropriate therapy is:
a) Adenosine
b) Amiodarone
c) Esmolol
d) Verapamil
e) Digoxin
REPEAT
d) Esmolol
Management of Arrhythmias After Heart Transplant
https://www.ahajournals.org/doi/10.1161/CIRCEP.120.007954
In asymptomatic patients, additional cardiac monitoring such as 24-Holter or an event monitor can be useful to assess the SVT burden, and a trial of atrioventricular nodal blockers (β-blockers preferably) can be attempted with caution in view of potential risk of bradycardia. Calcium channel blockers such as diltiazem and verapamil are contraindicated in patients taking immunosuppression such as tacrolimus and cyclosporine as it can impair the metabolism CYP3A, which increases the levels of these drugs potentially causing renal toxicity.
The use of adenosine in the management of SVT has remained a subject of controversy for over a quarter century. In the past, adenosine was contraindicated in patients post-OHT due to its supersensitivity and presumed risk of prolonged atrioventricular block.
Thus, based on the aforementioned data, in patients with OHT, adenosine is feasible and safe at reduced doses (starting at 1.5 mg for patients ≥60 kg) as long as patients are closely monitored, with dose escalation as needed. Furthermore, the 2010 American Heart Association guidelines on advanced cardiovascular life support also recommended lowering the initial dose of adenosine to 3 mg for the acute management of SVT in patients with OHT.
An 85-year-old is scheduled for open reduction and internal fixation of a fractured neck of femur today. They have no significant past medical history. Preoperative review including physical examination, full blood count, electrolyte profile and electrocardiogram performed yesterday were normal. In the anaesthetic bay, the monitor shows the patient to be in atrial fibrillation with a ventricular rate of 110 to 145 beats per minute. The blood pressure is 130/80 mmHg. The best initial treatment for the atrial fibrillation is:
A) Amiodarone
B) Metoprolol
C) Digoxin
D) Induce then cardiovert
E) Calcium Channel Blocker
B) Metoprolol
Guidelines from the American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC) recommend beta-blockers as a first-line therapy for rate control in atrial fibrillation.
Reference: January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2019;140(2)
NP A 65-year-old presents with an acute dissection of their thoracic aorta. Their blood pressure is 150/90 mmHg. The best medication to reduce the blood pressure is:
a) Esmolol
b) SNP
c) GTN
d) Hydralazine
A) esmolol
They get anti impulse therapy which usually starts off with beta blockade before alpha blockade.
Up to date: Patients often present with severe hypertension and are initially stabilized with fast-acting, intravenous beta blockers (eg, esmolol or labetalol) or calcium channel blockers. Anti-impulse therapy lowers blood pressure
A 30-year-old athlete undergoing a knee arthroscopy under general anaesthesia
develops intraoperative tachycardia. A 12-lead electrocardiogram is obtained and
shown below. The most likely diagnosis is:
a) AF
b) Flutter
c) AVNRT
d) Multifocal atrial tachycardia
AT
Repeat
Delta waves present, therefore WPW = AVRT
WPW + delta wave = AVRT → anatomical re-entry circuit (Bundle of Kent)
AVNRT is a functional re-entry circuit within the AV node
ECG features of AVNRT
● Regular tachycardia ~140-280 bpm
● Narrow QRS complexes (< 120ms) unless there is co-existing bundle branch block, accessory pathway, or rate-related aberrant conduction
● P waves if visible exhibit retrograde conduction with P-wave inversion in leads II, III, aVF. They may be buried within, visible after, or very rarely visible before the QRS complex
https://litfl.com/supraventricular-tachycardia-svt-ecg-library/
A third heart sound at the apex may be heard in:
a) Healthy people aged less than 40
b) Mitral prolapse
c) HTN
23.1 OPTIONS:
a) pulmonary stenosis
b) pulmonary hypertension
c) pericarditis
d) pregnancy
AT
Repeat
Can occur in healthy young people
The third heart sound is mainly created by the early-diastolic rapid distension of the left ventricle that accompanies rapid ventricular filling and abrupt deceleration of the atrioventricular blood flow
S3 may be normal in people under 40 years of age and some trained athletes but should disappear before middle age. Re-emergence of this sound late in life is abnormal[5] and may indicate serious problems such as heart failure.
‘Sounds like Ken-tu-cky’
The 12-lead electrocardiogram shown is most consistent with acute total occlusion
of the:
a) LAD
b) PDA
c) OM
d) RCA
VICTORIA
Am I missing something? I can’t see total occlusion of anything here.
Wellens syndrome- Lad
A 55-year-old with no past history of ischaemic heart disease is three days post-total hip replacement surgery. They have an episode of chest pain at rest with features typical of angina that lasts 30 minutes before fully resolving. There are no electrocardiogram changes and no troponin rise. The diagnosis is
a. No diagnosis made
b. Unstable angina
c. STEMI
d. NSTEMI
e. MINS
REPEAT
b. Unstable angina
UTD:
Unstable angina (UA) and acute non-ST elevation myocardial infarction (NSTEMI) differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury (troponins):
●UA is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponins, with or without electrocardiogram changes indicative of ischemia (eg, ST segment depression or transient elevation or new T wave inversion).
●NSTEMI is considered to be present in patients having the same manifestations as those in UA, but in whom an elevation in troponins is present.
MINS: Myocardial injury after non-cardiac surgery (up to 30 days post-op):
1. Elevated postop troponin
2. Resulting from myocardial ischaemia (i.e. no evidence of a non-ischaemic aetiology), not requiring an ischaemic feature (i.e. no chest pain, no ECG change)
VISION studies (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) demonstrated that severity of MINS strongly associated with 30-day mortality after NCS.
hs-cTnT
<20ng/L ~ 0.5% 30 day mortality
20-64ng/L ~3% 30 day mortality
65-999 ng/L ~9% 30 day mortality
>1000ng/L ~30% 30 day mortality
Whilst VISION trial identified MINS in at risk patients, the question now becomes what interventions are available to prevent this complication?
The QRS axis of the attached electrocardiograph is closest to:
a) -90
b) -45
c) +45
d) +90
VICTORIA
ECG sent to JJ
B
https://litfl.com/super-axis-man-sam/
Kate
In cardiac surgery a low-normal central venous pressure and a low blood pressure with a hyperdynamic heart is suggestive of:
a) Vasoplegia
b) Hypovolaemia
A) vasoplegia
Vasoplegia is characterized by a normal or augmented cardiac output with low systemic vascular resistance (SVR) causing organ hypoperfusion. The exact definition has varied but typically is considered when shock occurs within 24 h of CPB in the setting of a cardiac index (CI) is greater than 2.2 L/kg/m2 and SVR less than 800 dyne s/cm5
Kate
In an adult weighing 70 kg, a bedside assessment of haemodynamic status shows a left ventricular end-diastolic diameter of 2.4 cm. This finding suggests:
a) Hypovolaemia
b) Normal
c) Hypervolaemia
? Normal
Can only find absolute numbers or according to BSA not weight per se
Image
https://thoracickey.com/cardiac-chambers/
PSAX End diastolic AREA:
Hypovolemia <8cm2
Normal 8-14cm 2
Hypervolemia > 14cm2
IVSd and IVSs – Interventricular septal end diastole and end systole. The normal range is 0.6-1.1 cm.
LVIDd and LVIDs – Left ventricular internal diameter end diastole and end systole. The normal range for LVIDd is 3.5-5.6 cm, and the normal range for LVIDs is 2.0-4.0 cm.
LVPWd and LVPWs – Left ventricular posterior wall end diastole and end systole. The normal range is 0.6-1.1 cm.
RVDd – Right ventricular end diastole. The normal range is 0.7-2.3 cm.
Ao Root Diam – Aortic root diameter. The normal range is 2.0-4.0 cm.
LA Diameter – Left atrium diameter. The normal range is 2.0-4.0 cm.
The IVSd and IVPWd measurements are used to determine left ventricular hypertrophy, which is the thickening of the muscle of the left ventricle. LV hypertrophy is a marker for heart disease. In general, a measurement of 1.1-1.3 cm indicates mild hypertrophy, 1.4-1.6 cm indicates moderate hypertrophy, and 1.7 cm or more indicates severe hypertrophy.
Hypovolaemia
Normal for end diastole is 3.5 to 5.6cm
22.2 The most likely diagnosis for the following electrocardiograph is
(comment that this was like a 2015A repeat - ECG below is from that paper + 2022 recalled options)
a. AF with BBB
b. sinus tachy with BBB
c. ventricular tachycardia
d. torsades
b. sinus tachy with BBB
The most correct answer would be Trifasicular block:
RBBB with LAD (RBBB with left anterior hemiblock) and 1st degree heart block
Barash 8E 2017:
The term bifascicular block often refers to block in the right bundle and one of the two major fascicles of the left bundle. RBBB with left anterior hemiblock is present when the ECG shows an RBBB with a left axis deviation (usually greater than −60 degrees) in the absence of an inferior myocardial infarction. Complete RBBB with right axis deviation (greater than 90 degrees) is indicative of RBBB and left posterior hemiblock in the absence of a lateral myocardial infarction or evidence of right-sided heart failure. The term trifascicular block is used to describe first-degree AV block in the presence of bifascicular block.
Is it necessary to insert a temporary pacemaker before general anesthesia for an asymptomatic patient with bifascicular or trifascicular block?
The risk for progression to complete heart block in asymptomatic patients with bifascicular block is low. Further, no clinical characteristics have been identified that accurately predict the risk of development of complete heart block. Therefore, routine PPM implantation in patients with asymptomatic bifascicular block is not recommended. Observations made in the perioperative period have suggested that development of complete heart block during general anesthesia is also rare; therefore, it is generally not recommended that patients undergo temporary pacemaker insertion before general anesthesia. However, it is advisable to have an external pacemaker available in the operating room.
22.1 A four-year-old boy is in refractory ventricular fibrillation. The recommended dose of amiodarone is
80mg
Age + 4 x 2-> 4 + 4 x 2 =16kg
5 x 16mg =80mg
22.2 An absolute contraindication to transoesophageal echocardiography is
A. Dysphagia
B. GORD
C. Oesophageal stricture
D. oesophageal webbing
E. oesophageal varices
C. Oesophageal stricture
https://www.asecho.org/wp-content/uploads/2014/05/2013_Performing-Comprehensive-TEE.pdf
22.2 A four-year-old boy is in refractory ventricular fibrillation. The recommended dose of amiodarone is
a) 40mg
b) 80mg
c) 120mg
d) 160mg
80mg
Age + 4 x 2-> 4 + 4 x 2 =16kg
5 x 16mg =80mg
16kg x 5mg/kg = 80mg
20.1 In a Blalock–Taussig shunt, blood passes to the pulmonary artery via the
a. Aorta
b. Subclavian artery
c. IVC
d. SVC
e. Left atrium
B
23.1 Application of a pacemaker magnet to a dual-chamber implanted pacemaker would be expected to convert the operating mode to
a. AOO
b. VOO
c. DOO
d. AAI
c) DOO
The pacing mode will be DOO when the programmed pacing mode is a dual chamber mode or an MVP mode (AAIR<=>DDDR, AAI<=>DDD), VOO when the programmed pacing mode is a single chamber ventricular mode, and AOO when the programmed pacing mode is a single chamber atrial mode.
21.2 The image below on the left shows a normal central venous pressure (CVP) trace. The CVP
trace in the image below on the right is most consistent with
a) AF
b) MR
c) AR
d) TR
e) Pericardial constriction
TR
20.1 ECG calibration, 10mm on Y axis is equal to:
a. 0.2 sec
b. 0.4sec
c. 1sec
d. 0.1mV
e. 1mV
b) 1mV
22.1 A 68-year-old woman presents with a loud systolic murmur in the anaesthesia room before total
hip joint arthroplasty. A transthoracic echocardiogram is performed (image provided) and shows
a. AS
b. LVOT
c. MR
MR
21.2 Of the following, the lifestyle modification that is least effective in reducing essential
hypertension is
a) Stopping caffeine
b) Low salt diet
c) High potassium diet
d) Exercise
e) Alcohol cessation
a) Stopping caffeine
Eat a well-balanced diet that’s low in salt
Limit alcohol
Enjoy regular physical activity
Manage stress
Maintain a healthy weight
Quit smoking
Foods that are rich in potassium are important in managing high blood pressure (HBP or hypertension) because potassium lessens the effects of sodium. The more potassium you eat, the more sodium you lose through urine. Potassium also helps to ease tension in your blood vessel walls, which helps further lower blood pressure.
Source AHA
21.1 The management of a patient who has experienced a cardiac arrest within 10 days of cardiac surgery
should NOT routinely include
a. Atropine 3mg
b. adrenaline 1mg boluses
c. 3 stacked shocks
d. amiodarone 300
e. 1L fluid
b. adrenaline 1mg boluses
The risk of administering adrenaline in conventional doses is with profound hypertension, bleeding, or tearing of vessel anastomoses on return of spontaneous circulation (ROSC), which can precipitate catastrophic harm or further cardiac arrest.
Adrenaline remains a useful drug in peri-arrest situations in smaller doses.
23.1 The following is a chest X-ray from a patient complaining of dyspnoea after thoracic surgery. The diagnosis is
(not the image from the exam)
A. Dextracardia
B. Cardiac hernation
C. LLL collapse
D. Tension Pneumohorax
B. Cardiac hernation
https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.109.896829
20.2 A 56 year old patient presents with exertional syncope. The most likely diagnosis is
a) HOCM
b) Long QT
c) CCF
d) Myocardial ischaemia
HOCM if these remembered options are correct
Alternative is Aortic Stenosis which is more common than HOCM in this age group
20.2 Cardiovascular effects of hyperthyroidism include
a) Decreased CO
b) Increased PVR
c) Increased DBP
d) Decreased SVR
Decreased SVR
Hyperthyroidism:
increases HR
increases cardiac contractility.
increases LVEF
increases diastolic relaxation
increases CO
SVR decreases
>T3 induces systemic vasodilation.
20.2 According to National Audit Project (NAP) 5, the incidence of awareness during general anaesthesia for cardiac surgery is
a) 1:400
b) 1:800
c) 1:8000
d) 1: 12000
e) 1:20000
c) 1:8000
Awareness rates
GA with no muscle relaxant = 1:136,000
GA with muscle relaxation = 1/8,000
CTS 1/8,600
E-LSCS = 1/670
Overall 1:19,000
23.1 In order to minimise the risk of cardiac arrhythmia, surgical diathermy has been designed to operate with
A. High frequency
B. High amplitude
C. Low frequency
D. Low amplitude
E. Using EES
A. High frequency
22.2 Based on this ECG tracing, the mode in which this pacemaker is operating is
a) VAI with intermittent failure to capture
b) AAI with intermittent failure to sense
c) DDD
d) VVI with intermittent failure to capture
e) VVI with intermittent failure to sense
e) VVI with intermittent failure to sense
20.1 Cardiovascular effects of hyperthyroidism include
a) decreased diastolic relaxation
b) decreased SVR
c) decreased PVR
d) increased diastolic BP
Decreased SVR
- increased CO, increased SBP and decreased DBP with widened PP
Up to Date
Cardiovascular - Patients with hyperthyroidism have an increase in cardiac output, due both to increased peripheral oxygen needs and increased cardiac contractility. Heart rate is increased, pulse pressure is widened, and peripheral vascular resistance is decreased
22.2 A 45-year-old male received a heart transplant one month ago. He develops a new supraventricular tachyarrhythmia without hypotension during a gastroscopy. The most appropriate therapy is
a) Adenosine
b) Amiodarone
c) Digoxin
d) Esmolol
e) Verapamil
d) Esmolol
Management of Arrhythmias After Heart Transplant
https://www.ahajournals.org/doi/10.1161/CIRCEP.120.007954
In asymptomatic patients, additional cardiac monitoring such as 24-Holter or an event monitor can be useful to assess the SVT burden, and a trial of atrioventricular nodal blockers (β-blockers preferably) can be attempted with caution in view of potential risk of bradycardia. Calcium channel blockers such as diltiazem and verapamil are contraindicated in patients taking immunosuppression such as tacrolimus and cyclosporine as it can impair the metabolism CYP3A, which increases the levels of these drugs potentially causing renal toxicity.
The use of adenosine in the management of SVT has remained a subject of controversy for over a quarter century. In the past, adenosine was contraindicated in patients post-OHT due to its supersensitivity and presumed risk of prolonged atrioventricular block.
Thus, based on the aforementioned data, in patients with OHT, adenosine is feasible and safe at reduced doses (starting at 1.5 mg for patients ≥60 kg) as long as patients are closely monitored, with dose escalation as needed. Furthermore, the 2010 American Heart Association guidelines on advanced cardiovascular life support also recommended lowering the initial dose of adenosine to 3 mg for the acute management of SVT in patients with OHT.
22.1 A 74-year old man complains of chest pain. An electrocardiograph is performed and displayed here. The occluded coronary artery could be the
a) RCA or LCx
b) RCA
c) LAD
RCA or LCx
https://litfl.com/mi-localization-ecg-library/
22.1 A risk factor for the development of torsade de pointes is
a. hyperkalaemia
b. hypermagnasaemia
c. tachycardia
d. Female
d. Female
22.1 A drug which does NOT increase the defibrillation threshold in a patient with an implanted cardioverter defibrillator is
a. Amiodarone
b. Atropine
c. B-blocker
d. Flecainide
e. Sotalol
e. Sotalol
Drugs that INCREASE defibrillation threshold:
+ Amiodarone (Chronic)
+ Atropine
+ lignocaine
+ Diltiazem
+ Flecainide
+ Verapamil
+ Venlafaxine
+ Anaesthetic agents.
Drugs that DECREASE defibrillation threshold:
- Sotalol
- Amiodarone (acute)
- Nifekalant
Drugs with No Change in DFT
= B- blocker
= Disopyramide
= Procainamide
= Propafenone
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6304797/
23.1 Findings associated with massive pericardial tamponade include
a. Electrical alternans
b. Exaggerated collapsible IVC on ECHO during respiratory cycle
c. Pulses alternans
d. Kussmaul breathing
a) electrical alternans
Physical findings in Tamponade:
- A number of findings may be present on physical examination, depending upon the type and severity of cardiac tamponade
- None of the findings alone are highly sensitive or specific for the diagnosis.
Beck’s triad
1. Low arterial blood pressure
2. Dilated neck veins
3. Muffled heart sounds
- Are present in only a minority of cases of acute cardiac tamponade.
Diagnosis:
Clinical diagnosis is usually suspected based on the history and physical examination findings, which may include:
●Chest pain
●Syncope or presyncope
●Dyspnea and tachypnea
●Hypotension
●Tachycardia
●Peripheral edema
●Elevated jugular venous pressure
●Pulsus paradoxus
20.1 A patient with multiple co-morbidities has severe symptomatic aortic stenosis and is considered for an aortic valve replacement. Compared to an open surgical approach, a transcatheter aortic valve implantation (TAVI) has
a) Reduced vascular injury
b) Reduced mean valve gradient
c) Reduced paravalvular leak
d) Reduced complete heart block
e) Reduced reintervention
b) Reduced mean valve gradient
TAVI decreased:
- AKI
- AF
- Transfusion
- Mean prosthetic valve gradient
TAVI increased:
- Major vascular complications
- Permanent pacemaker implantation
- Paravalvular regurgitation
- Need for re-intervention
21.2 Of the following drugs, the least likely to cause pulmonary vasodilation when used at low
doses in patients with chronic pulmonary hypertension is
a) Dopamine
b) Dobutamine
c) Vasopressin
d) Milrinone
dopamine
- least likely to cause pulmonary vasodilation (all the others do to my knowledge)
- From UP TO DATE:
> At low doses of 1 to 3 mcg/kg per min, dopamine acts primarily on dopamine-1 receptors to dilate the renal and mesenteric artery beds
> At 3 to 10 mcg/kg per min (and perhaps also at lower doses), dopamine also stimulates beta-1 adrenergic receptors and increases cardiac output, predominantly by increasing stroke volume with variable effects on heart rate.
> At medium-to-high doses, dopamine also stimulates alpha-adrenergic receptors, although a small study suggested that renal arterial vasodilation and improvement in cardiac output may persist as the dopamine dose is titrated up to 10 mcg/kg per min
*clinically, the haemodynamic effects of dopamine demonstrate individual variability
Dobutamine (inodilator):
- selective β1-agonist that increases cardiac contractility and reduces pulmonary vascular and systemic vascular resistances
Vasopressin:
- vasopressin may have pulmonary vasodilatory effects in addition to a systemic vasoconstrictive effect
Milrinone (inodilator):
- the phosphodiesterase-3 inhibitors, milrinone and enxoimone, have positive inotropic effects combined with the capacity to reduce RV afterload (‘inodilators’) without significant chronotropic effect, but they can be associated with significant systemic hypotension
20.2 You are called to assist in the resuscitation of a 75-year-old female patient in the emergency department who is hypotensive and hypoxaemic in extremis. The image shown is of a focused transthoracic echocardiogram, parasternal short axis view. The most likely diagnosis is
a) Pulmonary embolism
b) Anterior MI
c) Cardiac tamponade
d) Pneumothorax
a) Pulmonary embolism
A bit about the RV in PE:
The right ventricle drapes around the LV. In response to an acute Pulmonary Embolus (PE) it first dilates. The RV can’t generate much force without training, sowhen the Pulmonary Vascular Resistance (PVR) first rises with a PE, thepulmonary arterypressures don’t actually rise substantially because the RV can’t generate largepressures.
Looking at the ventricle in short axis, the septum maybow towardstheLV which will form aD shape indiastole,producing a“volumeoverloaded right ventricle” appearance.
Only later whenthe RV has beentrainedwill it be able togenerate higher pressures. If the LV is D shaped insystole, this is a “pressureoverloaded right ventricle”.
Acute cor pulmonale with bothpressureANDvolumeoverload (D shape insystoleANDdiastole)is often absent.
20.1 You are inserting a pulmonary artery catheter in an intubated patient prior to cardiac surgery, and a significant amount of blood appears in the endotracheal tube. The most appropriate specific initial management is to:
A. Remove PAC and insert DLT
B. Wedge PAC and insert DLT
C. Wedge PAC and insert bronchial blocker
D. Withdraw PAC 2 cm and insert DLT
E. Withdraw PAC and insert bronchial blocker
F. Inflate balloon
D. Withdraw PAC 2 cm and insert DLT
LITFL: Pulmonary haemorrhage after PAOP measurement
a life threatening time-critical emergency pulmonary artery rupture caused by inflation of the pulmonary artery catheter (PAC) balloon during ‘wedging’ (measurement of the pulmonary artery occlusion pressure) some experts advise against measuring PAWP because of the risk of pulmonary artery rupture 0.2% risk, 30% mortality
RISK FACTORS
pulmonary hypertension mitral valve disease anticoagulants age >60 years
MANAGEMENT
Goals
prevent further pulmonary haemorrhage stop bleeding resuscitate
Call for help
ICU consultant anaesthetist/ OT cardiothoracic surgeon interventional radiology
Resuscitation
A may have to be emergently intubated if not already B FiO2 1.0 controlled ventilation if able to recognize which lung is haemorrhaging may be able to perform lung isolation (insert single lumen tube into unaffected side, exchange for a double lumen tube or use bronchial blocker with bronchoscopic assistance) apply PEEP to tamponade wound C large bore IV cannulae, fluids, blood products, inotropes
Specific therapy
Lay the patient ruptured side down withdraw pulmonary catheter 2-3 cm with balloon down then refloat PAC with balloon inflated to occlude pulmonary artery (to try to tamponade bleeding) stop antiplatelet agents and anticoagulants give reversal agents: — protamine for heparin — platelets for anti-platelet agents give blood products as indicated by FBC, coags and clinical state interventions — angiogram or bronchoscopy to isolate pulmonary vessel involved — if bleeding doesn’t settle will require lobectomy
21.2 A 30 year old athlete undergoing a knee arthroscopy under general anaesthesia becomes tachycardic intraoperatively. A 12-lead electrocardiogram (ECG) is obtained. The most likely diagnosis is
a) Atrial fibrillation
b) Atrial flutter
c) Sinus tachycardia
d) WPW
d) WPW
Type B pattern
LITFL:
ECG features of WPW in sinus rhythm
-> PR interval < 120ms
-> Delta wave: slurring slow rise of initial portion of the QRS
-> QRS prolongation > 110ms
-> Discordant ST-segment and T-wave changes (i.e. in the opposite direction to the major component of the QRS complex)
-> Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior infarction
Can be left-sided (Type A) or right-sided (Type B), and ECG features will vary depending on this:
Left-sided AP:
produces a positive delta wave in all precordial leads, with R/S > 1 in V1.
(Dominant R Wave in V1)
Sometimes referred to as a type A WPW pattern
Right-sided AP:
produces a negative delta wave in leads V1 and V2.
Sometimes referred to as a type B WPW pattern
Tachyarrhythmias in WPW
There are only two main forms of tachyarrhythmias that occur in patients with WPW
- Atrial fibrillation or flutter.
-> Due to direct conduction from atria to ventricles via an AP, bypassing the AV node - Atrioventricular re-entry tachycardia (AVRT).
-> Due to formation of a re-entry circuit involving the AP
Breakdown of Type A example:
- Sinus rhythm with a very short PR interval (< 120 ms)
- Broad QRS complexes with a slurred upstroke to the QRS complex — the delta wave
- Dominant R wave in V1 suggests a left-sided AP, and is sometimes referred to as “Type A” WPW
- Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy (RVH) — these changes are due to WPW and do not indicate underlying RVH
- Negative delta wave in aVL simulating the Q waves of lateral infarction — this is referred to as the “pseudo-infarction” pattern
23.1 Of the following drugs, the LEAST suitable for managing atrial arrhythmias in a patient with a left ventricular assist device is
A. Metoprolol
B. Amiodarone
C. Digoxin
D. Diltiazem
d) diltiazem
Nondihydropyridine calcium channel blockers should be used cautiously in patients with HFrEF because of their negative inotropic effects, and the role of these agents in LVAD recipients remains unclear
https://www.ahajournals.org/doi/10.1161/CIR.0000000000000673
Should also avoid sotolol
20.2 A 55 year old man with no past history of ischaemic heart disease is 3 days post total hip replacement surgery. He has an episode of chest pain that sounds ischaemic, began at rest and lasts thirty minutes before resolving fully. There are no ECG changes nor troponin rise. The diagnosis is
a. No diagnosis made
b. Unstable angina
c. STEMI
d. NSTEMI
e. MINS
b. Unstable angina
Not a Repeat, no Tropnin rise in this question making the answer unstable angina as opposed to NSTEMI
UTD:
Unstable angina (UA) and acute non-ST elevation myocardial infarction (NSTEMI) differ primarily in whether the ischemia is severe enough to cause sufficient myocardial damage to release detectable quantities of a marker of myocardial injury (troponins):
●UA is considered to be present in patients with ischemic symptoms suggestive of an ACS and no elevation in troponins, with or without electrocardiogram changes indicative of ischemia (eg, ST segment depression or transient elevation or new T wave inversion).
●NSTEMI is considered to be present in patients having the same manifestations as those in UA, but in whom an elevation in troponins is present.
MINS: Myocardial injury after non-cardiac surgery (up to 30 days post-op):
1. Elevated postop troponin
2. Resulting from myocardial ischaemia (i.e. no evidence of a non-ischaemic aetiology), not requiring an ischaemic feature (i.e. no chest pain, no ECG change)
VISION studies (Vascular Events in Noncardiac Surgery Patients Cohort Evaluation) demonstrated that severity of MINS strongly associated with 30-day mortality after NCS.
hs-cTnT
<20ng/L ~ 0.5% 30 day mortality
20-64ng/L ~3% 30 day mortality
65-999 ng/L ~9% 30 day mortality
>1000ng/L ~30% 30 day mortality
Whilst VISION trial identified MINS in at risk patients, the question now becomes what interventions are available to prevent this complication?
21.1 The 12 lead ECG shown (ECG with ST depression V1-V5, perhaps 1mm ste in lead 3) is most consistent with acute total occlusion of the
A. Posterior descending
B. RCA
C. LAD
D. OM
C. LAD
20.2 A 46-year old man collapses unexpectedly and fractures his femur. He is booked for acute theatre. A pre-operative electrocardiogram is performed. Of the following, the most appropriate peri-operative medical management is (ECG shown)
ECG = WPW
a) Flecainide
b) Aspirin
c) Digoxin
d) Magnesium
e) Verapamil
a) Flecanide
WPW ECG = short PR, wide QRS, delta wave at start of QRS
If WPW, need to prolong refractor period of accessory pathway with agents such as procainamide/flecainide/amiodarone/sotalol.
Avoid verapamil (increases ventricular rate).
Avoid beta blockers (don’t affect accessory pathway).
https://litfl.com/wolff-parkinson-white-syndrome-ccc/
21.2 An electrocardiogram (ECG) abnormality which is NOT usually associated with severe anorexia nervosa is
a) Sinus tachycardia
b) Wandering atrial pacemakers
c) ST depression
d) T wave inversion
e) Prolonged QT
a) Sinus tachycardia
BJA: Anorexia nervosa: perioperative implications
https://academic.oup.com/bjaed/article/9/2/61/299563
Cardiovascular
Typically anorexic patients are hypotensive and bradycardic. These physiological markers may be used as indications for hospitalization.
Bradycardia reflects the decrease in basal metabolic rate that arises as an adaptive response to starvation. Although patients are usually in sinus rhythm, electrocardiographic abnormalities are common and may be found in >80% of strict dieters. These include: atrioventricular block, ST depression, T wave inversion, and QT prolongation.
QT prolongation may be caused by hypocalcaemia, hypomagnesaemia, drugs, or directly by starvation itself. Electrolyte disturbances have a significant causal role in ECG abnormalities.
Other factors, for example, atypical antipsychotics, may also contribute.
Associated arrhythmias include: sinus arrest, wandering atrial pacemakers, nodal escape beats, supraventricular tachycardia, and ventricular tachycardia.
The reported incidence of arrhythmias under anaesthesia is 16–62%.
With respect to myocardial contractility, left ventricular function has been demonstrated to be impaired in a proportion of patients. Echocardiographic studies have also demonstrated a higher incidence of mitral valve prolapse in anorexic patients. The reasons for this are not entirely clear. It is postulated that the loss of left ventricular volume and mass leads to abnormal mitral valve motion.
In addition to starvation-induced myocardial impairment, the myocardium may be specifically damaged by pharmacological agents.
For example, emetogenic ipecac syrup is directly cardiomyotoxic and produces inflammatory changes and myocardial fibre degeneration when used long term.
Rarely, antipsychotic drugs, for example, olanzapine, may cause cardiomyopathy.
Myocardial impairment can be caused by hypophosphataemia which also reduces the threshold for arrhythmias.
Compromised myocardial function requires judicious use of fluids perioperatively as there is an increased risk of congestive cardiac failure. Echocardiography along with invasive perioperative monitoring (central venous catheter) should be considered to prevent fluid overload.
21.2 A 69-year-old woman has a recent onset of dyspnoea and undergoes a right heart catheterisation, with results displayed below. Her pulmonary capillary wedge pressure is 10 mmHg. The most likely diagnosis is
a) Mitral stenosis
b) Mitral regurgitation
c) Aortic stenosis
d) Pulmonary embolism
e) COPD
d) Pulmonary embolism
- fits with history of acute dyspnoea
- PCWP normal, therefore precapillary PH
- thus left heart disease unlikely to be the cause of elevated RVSP (clinical group 2)
- COPD possible if cor pulmonale, but this is an unlikely cause of acute dyspnoea given history
Normal PCWP excludes left heart disease as cause of pulmonary HTN (so not MR, MS or AS). The causes of pre-capillary pulm HTN are pulmonary arterial hypertension, pulmHTN secondary to lung disease, chronic thromboembolic pulmonaryHTN, pulmHTN with unclear/multifactorial mechanisms.
Normal pulmonary capillary wedge pressure = 8- 12mmHg
Normal PASP: 15-25mmHg
Normal PADP: 8-15mmHg
Pulmonary HTN is mPAP ≥25mmHg at rest. mPAP = PADP + (PASP-PADP/3)
mPAP in this image is 43 mmHg Transpulmonary gradient = mPAP – PAWP
20B
20B
20.1 The radial artery pressure trace shown below is from a patient who has an intra-aortic balloon pump in situ. The device has been switched to 1:2 augmentation to assess the timing. The trace shows an augmented beat followed by an un-augmented beat. With respect to the augmentation, the trace shows
a. Correct timing
b. Early inflation
c. Late inflation
d. Early deflation
e. Late deflation
Bonus question
b. Early inflation
Waveform features:
> Diastolic augmentation (peak B) encroaches on the peak corresponding to unassisted systole (peak A) – the two peaks have merged and are barely distinguishable.
> There is no ‘sharp V’ or dicrotic notch between peaks A and B.
Early IAB inflation may result in:
> Premature closure of the aortic valve and possible aortic regurgitation, thus impairing left ventricular emptying. There may be an increase in LVEDV, LVEDP and PCWP.
> Increased left ventricular wall stress (afterload) and increased myocardial oxygen consumption will occur.
how to correct:
Delay the onset of IAB inflation, so that it inflates at the dicrotic notch resulting in a ‘sharp V’ (see the normal pressure waveform).
During a routine preoperative examination of a patient’s heart, you note exaggerated splitting of the second heart sound with inspiration. This is characteristically heard in
A. Aortic Reguritation
B. HOCM
C. Left bundle branch block
D. Mitral Stenosis
E. Pulmonary Stenosis
E. Pulmonary Stenosis
DERANGED PHYSIOLOGY:
Splitting of the first heart sound
Right bundle branch block can produce a split first heart sound - because the contraction of the right ventricle is delayed- the conduction occurs via the left ventricle rather than the bundle of His- and thefore the closure of the tricuspid valve occurs after a substantial delay.
Atrial septal defect can result in a fixed split of the first heart sound
Splitting of the second heart sound
It is normal for this sound to be split. The high pressure in the systemic circulation slams the aortic valve shut rather abruptly, almost angrily. In contrast, low pressure of the pulmonary circulation tends to close the pulmonary valve gently, and therefore the pulmonary component of the second heart sound (P2) is usually delayed by about 20-30 milliseconds.
It is also normal for increased right ventricular filling to cause a widening of the split. The more blood in the RV, the longer it takes to eject, and therefore the greater the delay until pulmonary valve closure.
n the spontaneously breathing patient, the delay is greatest during inspiration. Naturally, in the patient ventilated with positive pressure the delay is greatest during expiration (positive pressure being a barrier to diastolic filling).
Increased normal splitting of S2
Anything that delays the end of right ventricular systole can cause this sort of picture.
Right bundle branch block - the delay in conduction via the left ventricle causes a delay in right ventricular contraction, and therefore a delay in pulmonary valve closure. The S1 will also be split.
Ventricular septal defect - because the right ventricle receives a large volume load directly from the left ventricle, and therefore takes longer to complete its systolic contraction.
Pulmonary valve stenosis - because the right ventricle takes longer to empty though a narrowed valve
Mitral regurgitation- not because right ventricular contraction is delayed, but because left ventricular contraction is shortened (as the LV empties in both the aortic and the atrial directuion, systole is over very quickly).
Fixed splitting of S2
Atrial septal defect - the atria, joined by a gaping hole in their seput, act as one atrium. The result is a reasonably equal distribution in volume betweent the right and left atrium. This way, both sides of the circulation share the same diastolic filling pressure. Dragging more volume into the right atrium with respiratory activity will not cause an inequality of ventricular filling (between the right and left ventricles) because the venous return will be “shared”.
Reversed splitting of S2
In this situation, P2 occurs before A2, and splitting widens during expiration (or inspiration in the mechanically ventilated patient). This only happens if the conduction to the left ventricle is delayed, or if the left ventricle is massively volume overload (and the right ventricle is not).
Left bundle branch block - the left ventricle depolarises after the right ventricle, and A2 is delayed
Aortic stenosis - the left ventricle empties slowly though a narrow valve
Large patent ductus arteriosus - the left ventricle receives a backflow of blood from the aorta, which causes it to become volume-overloaded
22.2 A 45-year-old man is ventilated in the intensive care unit and is in a critical state. His pulmonary artery wedge pressure is 26 mmHg, cardiac index is 1.7 L/minute/m2 and his PaO2/FiO2 ratio is 200 mmHg. A decision is made to place him on extracorporeal membrane oxygenation. The most appropriate mode is
a) VV ECMO
b) VA ECMO
c) Atrio-aorto ECMO
d) Ventriculo-atrial ECMO
b) VA ECMO
PaO2/FiO2 ratio
Mild: 200-300 = mortality 27%
Moderate = 100-200 mortality 32%
Severe < 100 = Mortality 45%
Cardiac Index
Normal: 2.5-4.2l/min
PAWP:
Normal 4-12mmHg
CI is low, PaO2/FiO2 ratio is mild, PAWP is high
23.1 A third heart sound at the apex may be heard in
a) pulmonary stenosis
b) pulmonary hypertension
c) pericarditis
d) pregnancy
d. pregnancy
21.2 A patient presents for a trans-urethral resection of the prostate (TURP). He had a single drug-eluting coronary stent for angina pectoris inserted six months ago and is taking clopidogrel and aspirin. The most appropriate preoperative management of his medications is to
a) Cease aspirin, continue clopidogrel
b) Cease aspirin for 10 days, cease clopidogrel for 5 days
c) Cease clopidogrel for 5 days, continue aspirin
d) Cease clopidogrel for 10 days, continue aspirin
e) Continue both aspirin and clopidogrel
c) Cease clopidogrel for 5 days, continue aspirin
- prostatic surgery, the risk of major bleeding may be greater than the risk of stent thrombosis
- For clopidogrel, we stop five days before surgery
- Clopidogrel, if stopped, should be restarted with a loading dose of 300 mg as soon as possible after surgery, perhaps later in the day if postoperative bleeding has stopped. Some experts recommend a higher loading dose of 600 mg to decrease time to effectiveness in the higher-risk postoperative setting
- suggest that surgery be performed in centers with 24-hour interventional cardiology coverage
UP TO DATE: Noncardiac surgery after PCI
Nonemergency noncardiac surgery — For patients who have undergone previous stenting with either BMS or DES and who will need cessation of one or both antiplatelet agents, we prefer to defer planned nonemergency, nonurgent noncardiac surgery until at least six months after stent implantation. The risks of noncardiac surgery before six months are increased after both BMS and DES.
For patients whose surgery requires cessation of one or both antiplatelet agents and cannot wait six months, and where the risks of delaying surgery outweigh the benefits, our recommended minimal duration of DAPT is four to six weeks, depending on the urgency of surgery and risk of thrombotic complication. This is based in part on evidence suggesting that the increased risk of MI and cardiac death is highest within the first month after stent placement and no clear difference in risk between BMS and DES. Although we prefer to wait at least six weeks when possible, in patients for whom earlier surgery is in their best interest after weighing risks and benefits, we sometimes refer patients as early as four weeks after stent placement.
The proinflammatory and prothrombotic risks of surgery may increase the baseline risk of stent thrombosis even in the presence of DAPT and regardless of stent type during this early period after stenting. We believe this risk to be higher prior to the minimum duration of DAPT recommended above, but the final decision to continue or discontinue antiplatelet therapy in the perioperative period should be made only after an informed discussion among the surgeon, managing cardiologist (and other health care providers), and patient has taken place. In many cases, DAPT can be continued in the perioperative period, although for some surgeries, such as neurosurgery, posterior eye surgery, or prostatic surgery, the risk of major bleeding may be greater than the risk of stent thrombosis.
In these patients who undergo noncardiac surgery before the recommended minimum duration of DAPT, a platelet P2Y12 receptor blocker should be discontinued for as brief a period as possible. Aspirin should be continued through the perioperative period, since the risk of stent thrombosis is further increased with the cessation of both aspirin and clopidogrel and surgery can usually be safely performed on aspirin. The rationale to continue aspirin comes in part from the POISE-2 trial (PCI subgroup analysis), which is discussed separately. However, as many neurosurgical patients, for whom bleeding might be life threatening or lead to severe adverse outcomes, were not enrolled in POISE-2, the optimal strategy is not known.
●Minor surgical and dental procedures usually do not require cessation of antiplatelet therapy.
●With regard to stopping P2Y12 inhibitor prior to noncardiac surgery, we generally follow recommendations found in the manufacturer’s package insert for each drug.
- For clopidogrel, we stop five days before surgery; that is, the last dose is taken on the sixth day before surgery.
- For prasugrel, we stop seven days before surgery.
- For ticagrelor, we stop three to five days before surgery.
- Some experts are willing to recommend shorter discontinuation periods for procedures less likely to be associated with major bleeding.
●Clopidogrel, if stopped, should be restarted with a loading dose of 300 mg as soon as possible after surgery, perhaps later in the day if postoperative bleeding has stopped. Some experts recommend a higher loading dose of 600 mg to decrease time to effectiveness in the higher-risk postoperative setting.
●We suggest that surgery be performed in centers with 24-hour interventional cardiology coverage
23.1 A patient presents for a transurethral resection of the prostate (TURP). He had a single drug-eluting coronary stent for angina pectoris inserted six months ago and is taking clopidogrel and aspirin. The most appropriate preoperative management of his medications is to
a) Cease aspirin, continue clopidogrel
b) Cease aspirin for 10 days, cease clopidogrel for 5 days
c) Cease clopidogrel for 5 days, continue aspirin
d) Cease clopidogrel for 10 days, continue aspirin
e) Continue both aspirin and clopidogrel
C) Cease clopidogrel for 5 days, continue aspirin
WFSA update document
https://resources.wfsahq.org/wp-content/uploads/uia29-Perioperative-management-of-patients-with-coronary-stents-for-non-cardiac-surgery.pdf
Dual antiplatelet therapy should be continued in all patients with coronary stents presenting for surgery.
However, if there is a high risk of surgical bleeding then clopidogrel should be stopped 5-7 days before surgery and monotherapy with aspirin should be continued.
Clopidogrel should be restarted as soon as possible post surgery. Cessation of aspirin therapy may be considered during intracranial surgery and transuretheral resection of prostrate as these procedures are associated with an increased risk of bleeding, but only after contemplating the risk-benefit ratio.
2014 AHA/ACC guidelines on perioperative medicine don’t give a firm answer except: > 180 days since insertion = proceed (Level II b evidence)
22.1 A 26-year-old patient presents with exertional syncope. The most likely diagnosis is
a. HOCM
b. Long QT syndrome
c. CCF
d. IHD
HOCM: pathopneumonic
A person who has syncope during exertion is more likely to have an obstruction to blood flow (aortic stenosis or hypertrophic cardiomyopathy) or ventricular tachycardia as a cause. On the other hand, syncope after completion of exercise is more likely of reflex origin, such as the common faint.
https://www.uptodate.com/contents/syncope-fainting-beyond-the-basics#:~:text=A%20person%20who%20has%20syncope,such%20as%20the%20common%20faint
23.1 You are called to assist in the resuscitation of a 75-year-old patient in the emergency
department who is in extremis with severe hypotension and hypoxaemia. The image
shown is of a focused transthoracic echocardiogram, parasternal short axis view.
The most likely diagnosis is
a. PE
b. Tamponade
a) PE
D-shaped left ventricle
22.2 You are inserting a pulmonary artery catheter in an intubated patient prior to cardiac surgery and a significant amount of blood appears in the endotracheal tube. The most appropriate specific initial management is to
a. Remove PAC and insert DLT
b. Wedge PAC and insert BB
c. Wedge PAC and insert DLT
d. Withdraw PAC 2cm and insert DLT
d. Withdraw PAC 2cm and insert DLT
Pulmonary rupture
Miller:
- Position pt with bleeding lung dependent
- Perform endotracheal intubation, oxygenation, airway toilet
- Isolate lung by endobronchial DLT or SLT or bronchial blocker
- Withdraw PAC several centimetres, leaving it in the main PA. Do not inflate the balloon (except with fluoroscopic guidance)
- Position pt with isolated bleeding lung nondependent. Administer PEEP to the bleeding lung if possible
- Transport the patient to medical imaging for diagnosis and embolisation if feasible