Cardiac surgery and interventional cardiology Flashcards

Question

The QRS axis of the attached electrocardiograph is closest to: a) -90 b) -45 c) +45 d) +90

Answer 1

VICTORIA ECG sent to JJ B https://litfl.com/super-axis-man-sam/

Answer 2

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

Answer 3

? 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

Answer 4

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.

Answer 5

80mg Age + 4 x 2-> 4 + 4 x 2 =16kg 5 x 16mg =80mg

Answer 6

C. Oesophageal stricture ## Footnote https://www.asecho.org/wp-content/uploads/2014/05/2013_Performing-Comprehensive-TEE.pdf

Answer 7

80mg Age + 4 x 2-> 4 + 4 x 2 =16kg 5 x 16mg =80mg | 16kg x 5mg/kg = 80mg

Answer 8

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.

Answer 9

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

Answer 10

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.

Answer 11

B. Cardiac hernation https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.109.896829

Answer 12

HOCM if these remembered options are correct Alternative is Aortic Stenosis which is more common than HOCM in this age group

Answer 13

Decreased SVR Hyperthyroidism: increases HR increases cardiac contractility. increases LVEF increases diastolic relaxation increases CO SVR decreases >T3 induces systemic vasodilation.

Answer 14

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

Answer 15

A. High frequency

Answer 16

e) VVI with intermittent failure to sense

Answer 17

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

Answer 18

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.

Answer 19

RCA or LCx https://litfl.com/mi-localization-ecg-library/

Answer 20

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/

Answer 21

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

Answer 22

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

Answer 23

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

Answer 24

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, so when the Pulmonary Vascular Resistance (PVR) first rises with a PE, the pulmonary artery pressures don’t actually rise substantially because the RV can’t generate large pressures. Looking at the ventricle in short axis, the septum may bow towards the LV which will form a D shape in diastole, producing a “volume overloaded right ventricle” appearance. Only later when the RV has been trained will it be able to generate higher pressures. If the LV is D shaped in systole, this is a “pressure overloaded right ventricle”. Acute cor pulmonale with both pressure AND volume overload (D shape in systole AND diastole) is often absent.

Answer 25

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

Answer 26

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 1. Atrial fibrillation or flutter. -> Due to direct conduction from atria to ventricles via an AP, bypassing the AV node 2. 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

Answer 27

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

Answer 28

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?

Answer 29

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/

Answer 30

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.

Answer 31

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

Answer 32

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).

Answer 33

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

Answer 34

b) VA ECMO | CI is low, PaO2/FiO2 ratio is mild, PAWP is high 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

Answer 35

d. pregnancy

Answer 36

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

Answer 37

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)

Answer 38

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

Answer 39

a) PE D-shaped left ventricle

Answer 40

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

Answer 41

Warm ischaemia time: - Time from treatment withdrawal to the start of cold perfusion of the donated organs - Significance is the impact on graft function - Most important phase of WIT begins when the systolic BP is < 60mmHg - This includes the waiting period from the absence of circulation to the declaration of death and the time before initiating the flow of cold perfusate through the cannula Maximum WARM Ischaemia time - Heart 30 mins - Liver 30 mins - Pancreas 30 mins - Kidney 60 mins - Lungs 90 mins Maximum COLD Ischaemia time: - Heart = 4 hrs - Lungs = 6-8hrs - Liver/Pancreas = 12hrs (DBD)/6 hrs (DCD) - Kidneys = 18hrs (DBD)/ 12 hrs (DCD)

Answer 42

e) Decreased SVR - increased CO, increased SBP and decreased DBP with widened PP UP TO DATE: Cardiovascular effects of hyperthyroidism: - Thyroid hormone has important effects on cardiac muscle, the peripheral circulation, and the sympathetic nervous system that alter cardiovascular hemodynamics in a predictable way in patients with hyperthyroidism. - The main changes are : ●Increases in heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption ●Reductions in systemic vascular resistance and diastolic pressure

Answer 43

c) 93% ANZCOR suggests against the routine administration of oxygen in persons with chest pain.13 [2015 COSTR, weak recommendation, very-low certainty evidence] For persons with heart attack, routine use of oxygen is not recommended if the oxygen saturation is >93% [National Heart Foundation of Australia & Cardiac Society of Australia and New Zealand: practice advice].9

Answer 44

d. Early deflation https://litfl.com/intra-aortic-balloon-pump-trouble-shooting/ Waveform features: > There is a sharp drop in pressure immediately following the peak of diastolic augmentation (peak B). > Diastolic augmentation may be suboptimal but it is difficult to confirm in the absence of a pressure scale or comparison to an unassisted waveform. > Assisted aortic end-diastolic BP may be sub-optimally increased (trough C), but it is difficult to say based on the information given. With early deflation a widened U-shaped trough is typically seen. > Early deflation can lead to an assisted aortic end-diastolic BP that equals or exceeds the unassisted aortic end-diastolic BP (trough F), although this is not the case in this scenario. > Assisted SBP (peak D) is the same or higher than the unassisted SBP (peak A) – it should be slightly less. Early IAB deflation may result in: > inadequate coronary perfusion, with the potential for retrograde coronary blood flow. This may result in angina due to decreased myocardial oxygen supply. > suboptimal afterload reduction and increased myocardial oxygen demand How to correct: Prolong the IAB inflation time, so that it deflates at the end of diastole, just before the onset of isovolumetric systolic contraction.

Answer 45

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.

Answer 46

a) Bleeding ECMO complications: - patient complications: bleeding & coagulopathy most common - mechanical complications: access insufficiency common Blue book 2017

Answer 47

d. Noradrenaline Supportive Management of Massive PE Coexisting left ventricular systolic dysfunction and diastolic dysfunction complicate the management of heart failure patients with massive PE. Although a common strategy in response to systemic arterial hypotension is to prescribe a fluid bolus, volume loading may worsen biventricular failure, pulmonary edema, and hypoxemia. An initial trial of volume expansion, limited to 250 to 500 mL, may be attempted in those heart failure patients without evidence of increased right-sided filling pressures or pulmonary edema.6 Although non–heart failure patients generally respond well to pure vasopressors for hemodynamic support in massive PE, many heart failure patients will not tolerate the isolated increase in systemic vascular resistance. PE patients with heart failure may require an agent with mixed vasopressor and inotropic properties such as norepinephrine, epinephrine, or dopamine. Whereas LV function often becomes hyperdynamic to compensate for RV failure, the presence of underlying LV systolic dysfunction in heart failure patients may limit the patient’s ability to maintain normal systemic cardiac output and may necessitate the addition of inotropes. https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.108.803965

Answer 48

e) Decreased 40% Infra-renal aortic cross-clamping leads to a reduction in renal blood flow by up to 40%, as a result of an increase in renal vascular resistance of up to 75%. The mechanism underlying this increased resistance is uncertain but may, in part, be a result of the associated decrease in cardiac output during aortic cross-clamping, as well as because of humoral mechanisms, which lead to increased release of renin. After declamping, there is a maldistribution of renal blood flow away from the cortex for at least 60 min.

Answer 49

c) Vasopressin https://emcrit.org/ibcc/pressors/ - 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

Answer 50

A Couldn't find a clear source but we know; A - will decrease venoplegia and improve venous return B - Would not help, decrease VR C - Don't drop FiO2 when desatting... D - increases PVR (unless below FRC) and reduces pulmonary flow E - Same as above, increased PVR and reduces flow through pulmonary circuit B. Decreasing the ventilator tidal volumes. 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.

Answer 51

R-wave peak

Answer 52

increased SVR EMSB handbook CO is reduced after Burn injury 2ry to: - myocardial depressant mediators - decreased blood volume - reduced venous return - increased pulmonary and systemic vascular resistance due to increased levels of catecholamines In the first 24hrs reduced cardiac output persists even after restoration of blood volume Between 24-48hrs post burn a hyperdynamic state develops with reduced peripheral resistance, increased oxygen consumption and increased cardiac output

Answer 53

d) 100 x PPmax - PPmin / PPmean

Answer 54

A. Magnesium TdP UTD - BB specifically propanolol or nadolol if Hx of syncope / seizures or resus SCA ## Footnote https://www.uptodate.com/contents/congenital-long-qt-syndrome-treatment

Answer 55

A. Digitalis toxicity Miller’s The ECG made easy http://lifeinthefastlane.com/ecg-library/pmi/ Normal Q waves - Due to depolarisation of the interventricular septum from left to right - Seen in the left-sided leads (I, aVL, V5, V6) Pathological Q waves - > 1 mm depth - > 1 mm (= 40 ms) across Digoxin ECG changes - Therapeutic: prolonged PR interval (AV nodal delay), shortened QTC intervals (rapid ventricular repolarisation), ST depression (↓ slope of phase 3), T wave inversion - Toxic: atrial or ventricular arrhythmias (↑ automaticity), prolonged PR interval → heart block, SA node inhibition → sinus arrest - Atrial tachycardia with block = most common arrhythmia attributed to digoxin toxicity - VF = most frequent cause of death - QRS = normal! Q waves in MI - Occur with transmural infarctions, and are less likely with subendocardial infarctions - Develops days after the onset of AMI, and is usually permanent - Indicates the part of the heart that has been damaged LBBB ECG changes - Wide QRS - Wide QS complex in lead V1 - Wide R wave in lead V6 with slight notching at the peak and TWI - The axis is highly variable: can be normal or deviated to the left or right Wolff-Parkinson-White syndrome - Due to the presence of an accessory bundle between the atrium and ventricle, which has no AV node to delay conduction - Short PR interval - Early slurred upstroke of the QRS complex due to delta wave

Answer 56

b. AR https://litfl.com/oesophageal-doppler/

Answer 57

C. Between lowest renal artery to bifurcation of aorta https://litfl.com/reboa-in-resuscitation/ Anatomy: The aorta is divided into three separate zones for the purposes of REBOA (aortic length varies between individuals) Zone I of the aorta extends from the origin of the left subclavian artery to the coeliac artery (approx 20cm long in a young adult male) Zone II extends from the coeliac artery to the most caudal renal artery (approx 3cm long) Zone III extends distally from the most caudal renal artery to the aortic bifurcation (approx 10cm long) REBOA location based on injury: >suspected or diagnosed intra-abdominal haemorrhage due to blunt trauma or penetrating torso injuries (Zone I REBOA), or >blunt trauma patients with suspected pelvic fracture and isolated pelvic haemorrhage (Zone III REBOA), or >patients with penetrating injury to the pelvic or groin area with uncontrolled haemorrhage from a junctional vascular injury (iliac or common femoral vessels) (Zone III REBOA) Simplistic rendering of aorta. Zone 1 (from left subclavian artery to the upper border of the celiac trunk), Zone 2 (the upper border of the celiac trunk to the lower border of the distal take-off of the renal arteries), and Zone 3 (from the lower border of the lower renal artery to the aortic bifurcation). Zone 1 is occluded in the case of cardiac arrest or life-threatening intra-abdominal hemorrhage; Zone 2 has no current indication; and Zone 3 is occluded in the case of life-threatening pelvic or lower limb haemorrhage7. REBOA Resuscitative Endovascular Balloon Occlusion of the Aorta.

Answer 58

Bonus question e. Late deflation https://litfl.com/intra-aortic-balloon-pump-trouble-shooting/ Waveform features: > The peak corresponding to diastolic augmentation (peak C) is widened. > Assisted aortic end-diastolic BP (trough E) is the same as, not lower than, the unassisted aortic end-diastolic BP (trough G). > The upstroke of assisted systolic BP (peak F) has a gentle gradient resulting in a prolonged rise. Late deflation of the IAB has these effects: > There is no afterload reduction. The inflated balloon may actually impede left ventricular ejection and increase the afterload. > Myocardial oxygen consumption will increase because the left ventricle experiences a longer period of isovolumetric contraction (when most myocardial oxygen consumption occurs) and has to contract against greater resistance (afterload). How to correct: > Shorten the IAB inflation time, so that the IAB deflates at the end of diastole – just before isovolumetric contraction of the left ventricle.

Answer 59

? no recalled ? MPAP – PCWP = Transpulmonary gradient 27mmHg TPG = mPAP – PCWP

Answer 60

Warm ischaemia time: - Time from treatment withdrawal to the start of cold perfusion of the donated organs - Significance is the impact on graft function - Most important phase of WIT begins when the systolic BP is < 60mmHg - This includes the waiting period from the absence of circulation to the declaration of death and the time before initiating the flow of cold perfusate through the cannula Maximum WARM Ischaemia time - Heart 30 mins - Liver 30 mins - Pancreas 30 mins - Kidney 60 mins - Lungs 90 mins Maximum COLD Ischaemia time: - Heart = 4 hrs - Lungs = 6-8hrs - Liver/Pancreas = 12hrs (DBD)/6 hrs (DCD) - Kidneys = 18hrs (DBD)/ 12 hrs (DCD)

Answer 61

decreased SVR Hyperthyroidism causes a hyperdynamic circulation, characterized by increased cardiac contractility and heart rate, increased preload, and decreased systemic vascular resistance (SVR), resulting in significantly increased cardiac output https://www.sciencedirect.com/science/article/pii/S0735109718333795#:~:text=Hyperthyroidism%20causes%20a%20hyperdynamic%20circulation,in%20significantly%20increased%20cardiac%20output.

Answer 62

MR?? See UpToDate PAC interpreting

Answer 63

b. valsalva Fluid and magnesium - fixes all. But could also be conscious VT or something stupid....

Answer 64

VA ecmo VA - bleeding (large bore arterial puncture)

Answer 65

Answer: e) Bernoulli equation using tricuspid peak + RAP i.e. RVSP = 4v2 + RAP (~PAP in absence of RVOTO)

Answer 66

) Hypertension Talley & O'Connor CVS Exam: S3: Physiological in pregnancy; sign of LV failure; AR & MR S4: Never physiological, most often due to systemic hypertension Atrial gallop - stiff LV - hypertrophy or ischaemic ventricle Source CV phys

Answer 67

RCA Source: LITFL RCA occlusion is suggested by: ST elevation in lead III > lead II Presence of reciprocal ST depression in lead I Signs of right ventricular infarction: STE in V1 and V4R

Answer 68

= ΔP = 4v2 = 4 x 9 = 36

Answer 69

a. Bleeding repeat

Answer 70

RWMA Echocardiographic images recorded during ischemia show abnormalities of wall motion, thus allowing for the detection of significant coronary artery disease https://www.sciencedirect.com/topics/nursing-and-health-professions/stress-echocardiography

Answer 71

Dilated RA and RV

Answer 72

Bonus question a. Correct timing https://derangedphysiology.com/main/required-reading/cardiothoracic-intensive-care/Chapter%20634/normal-iabp-waveform

Answer 73

a) 41mmHg Answer: RVSP = 4v2 + CVP 4x3x3+5 = 41

Answer 74

a) <1% low risk for 30 day adverse cardiovascular event. >5% high. 1-5% therefore moderate. https://www.ahajournals.org/doi/10.1161/circ.105.10.1257 Based on surgery type c) 10-15% (unlikely this) Based on patient factors alone, adults can be categorized into low (<5%), borderline (5 to <7.5%), intermediate (≥7.5 to <20%), or high (≥20%) 10-year CVD risk. Source: ACC/AHA Guideline 2019 https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2019/03/07/16/00/2019-acc-aha-guideline-on-primary-prevention-gl-prevention https://www.jacc.org/doi/epdf/10.1016/j.jacc.2019.03.010

Answer 75

C. MINS (Anthony reckons) B. NSTEMI https://resources.wfsahq.org/atotw/perioperative-myocardial-ischaemia-in-non-cardiac-surgery/ MI is defined as myocardial cell death due to prolonged myocardial ischaemia. It is diagnosed by22 a rise of cardiac biomarker value above the 99th percentile limit with at least 1 of the following: 1. Symptoms of ischaemia, 2. New ST-segment T wave changes or new left bundle branch block, 3. New pathological Q waves, 4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality 5. Identification of an intracoronary thrombus by angiography or autopsy OR: Cardiac death with symptoms suggestive of myocardial ischaemia. It is important to note that the above diagnostic criteria have not been created for the perioperative setting. An elevated troponin after noncardiac surgery, even without other features of ischaemia independently increases the risk of 30-day mortality.21 With this in mind, a new perioperative diagnosis has been created—myocardial injury after noncardiac surgery (MINS). MINS is diagnosed by a postoperative peak troponin T of 0.03 ng/mL or greater due to myocardial ischaemia.21 Although a diagnosis of MINS has prognostic significance, the clinical utility remains uncertain. MINS is defined as myocardial cell injury during the first 30 days after noncardiac surgery due to an ischemic etiology (ie, no evidence of a nonischemic etiology like sepsis, rapid atrial fibrillation, pulmonary embolism, cardioversion, chronically elevated troponin, etc) and is independently associated with mortality. MINS includes MI (both symptomatic and non-symptomatic) and patients with postoperative elevations in troponin but who do not have symptoms, electrocardiographic abnormalities, or other criteria that meet the universal definition described above, and have no evidence of a nonischemic etiology for their troponin elevation) Circulation https://www.ahajournals.org/doi/10.1161/CIR.0000000000001024 MINS includes myocardial infarction and ischemic myocardial injury that do not fulfill the Universal Definition of Myocardial Infarction (myocardial injury with a rise or fall of cTn above the 99th percentile of the upper reference limit and at least 1 of the following: ischemic symptoms, new ischemic electrocardiographic changes, development of new pathological Q waves on ECG, imaging evidence of myocardial ischemia, or angiographic or autopsy evidence of coronary thrombus). MINS is defined by at least 1 postoperative cTn concentration that exceeds the 99th percentile upper reference limit of the cTn assay as a result of a presumed ischemic mechanism (ie, supply-demand mismatch or atherothrombosis) in the absence of overt nonischemic causes (eg, pulmonary embolus; Table 1). Such elevations in cTn must be identified within the first 30 days after surgery but nearly always occur within the first 2 postoperative days. Clinical symptoms and electrocardiographic changes are not required to establish a diagnosis of MINS, which includes myocardial infarction and ischemic myocardial injury.

Answer 76

b) Adrenaline -You do not use full dose adrenaline (rather, give smaller doses) -You do three "stacked shocks" -You try pacing (rate of 90, DDD) in asystole if pacing wires are available -If they are already paced and in PEA, you turn off the pacing to "unmask" VF. -These shocks and attempted pacing are all measures you take before starting CPR, which is a departure from the ACLS norms. -If you can't control a shockable rhythm with three stacked shocks, you give amiodarone immediately rather than after three cycles. -Amiodarone is the only drug in the protocol, which makes it easy to remember. - -After five minutes of unsuccessful resuscitation the chest should be re-opened. ---External CPR is pointless in all of the common causes of arrest in this scenario. Therefore, CPR is something you do while waiting to re-open the chest. -Non-surgical staff are encouraged to re-open the chest in an emergency ## Footnote https://derangedphysiology.com/main/required-reading/cardiac-arrest-and-resuscitation/Chapter%20221/cardiac-arrest-following-cardiac-surgery

Answer 77

C. 3 - if male CHA2DS2-VASc score ≥2 to be recommended chronic OAC (Grade 1A). - if female CHA2DS2-VASc score ≥3 to be recommended chronic OAC (Grade 1A). * non-sex risk factor also holds bearing: - For patients with CHA2DS2-VASc score of 1 in males and 2 in females based on age 65 to 74 years, we recommend chronic OAC (Grade 1A). Up to date: Our approach to deciding whether to prescribe anticoagulant therapy for patients with AF (excluding those with rheumatic mitral stenosis that is severe or clinically significant [mitral valve area ≤1.5 cm2], a bioprosthetic valve [surgical or bioprosthetic] within the first three to six months after implantation, or a mechanical heart valve) is as follows: *For a CHA2DS2-VASc score ≥2 in males or ≥3 in females, we recommend chronic OAC (Grade 1A). *For a CHA2DS2-VASc score of 1 in males and 2 in females: -For patients with CHA2DS2-VASc score of 1 in males and 2 in females based on age 65 to 74 years, we recommend chronic OAC (Grade 1A). Age 65 to 74 years is a stronger risk factor than the other factors conferring one CHA2DS2-VASc score point. -For patients with other risk factors, the decision to anticoagulate is based upon the specific nonsex risk factor and the burden of AF. For patients with very low burden of AF (eg, AF that is well documented as limited to an isolated episode that may have been due to a reversible cause such as recent surgery, heavy alcohol ingestion, or sleep deprivation), it may be reasonable to forgo chronic OAC and institute close surveillance for recurrent AF, although it may not be possible to reliably estimate AF burden from surveying symptoms or infrequent monitoring. The frequency and duration of AF episodes vary widely over time, and episodes are often asymptomatic. *For patients with a CHA2DS2-VASc of 0 in males or 1 in females, we suggest against OAC (Grade 2C). Patient values and preferences may impact the decision. For example, a patient who is particularly stroke averse and is not at increased risk for bleeding may reasonably choose anticoagulation, particularly if the patient is a candidate for treatment with a direct oral anticoagulant (DOAC). 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline

Answer 78

Chronic obstructive pulmonary disease (COPD) is the most common cause of cor pulmonale leads to an increase in RV afterload secondary to changes in pulmonary vascular structure and mechanics, and lung hyperinflation. Patients with COPD who subsequently develop RV dysfunction have an increased risk of admission to hospital and mortality

Answer 79

c) ASD closure device Amplatzer Device

Answer 80

c) LAD LIFL: Myocardial Ischaemia https://litfl.com/myocardial-ischaemia-ecg-library/ More Myocardial Ischaemia ECG Examples: Example 1 Subendocardial ischaemia: The most striking abnormality is the widespread ST depression, seen in leads I, II and V5-6. This is consistent with widespread subendocardial ischaemia. There is also some subtle ST elevation in V1-2 and aVR with small Q waves in V1-2, suggesting that the cause of the widespread ischaemia is a proximal LAD occlusion.

Answer 81

c) Increased mortality Use of perioperative metoprolol was associated with: * Decreased rate of myocardial infarction * Decreased rate of revascularisation * Decreased rate of developing new atrial fibrillation * INCREASED rate of death * INCREASED rate of stroke * INCREASED rate of significant hypotension INCREASED rate of significant bradycardia

Answer 82

Aortic stenosis

Answer 83

b) Aortic Stenosis

Answer 84

b) vasoplegia

Answer 85

e. VOO >Asynchronous mode most often the result of magnet application. In a ventricular PPM, this means VOO >However, various sources recommend against use of magnet for PPM management due to inconsistent effects on different devices Equipment in Anaesthesia and Critical Care: > The use of a magnet as a solution for pacemaker problems, either in theatre or otherwise is not recommended. >The application of a magnet to the pacemaker can have unpredictable results, from causing it to change to a back-up mode such as VOO, to reverting to factory settings, to performing various self-tests, to switching off entirely.

Answer 86

B. Programability ? Multi-site pacing?

Answer 87

B. 2 ( CVA, Insulin use) ## Footnote UTD CHF Renal impairment Insulin use Stroke Ischaemic heart Surgically high risk

Answer 88

d) Alprostadil https://www.rch.org.au/piper/neonatal_medication_guidelines/Alprostadil_(Prostin_VR)_%E2%80%93_(Prostaglandin_E1)/ Alprostadil (PROSTAGLANDIN E1) is a synthetic prostaglandin used to relax the ductus arteriosus in early post-natal life, where a patent ductus is critical for survival, including Tetralogy of Fallot, pulmonary atresia, pulmonary stenosis, tricuspid atresia and transposition of the great arteries. Dose To open a closed ductus arteriosus: 0.1 micrograms/kg/minute (100 nanograms/kg/min). An effect is usually seen within 30-60 minutes. Reduce the dose once an effect is seen or as directed by a Consultant.1 Doses > 0.1 micrograms/kg/minute are rarely more effective and may cause serious adverse effects.3 To maintain patency of ductus arteriosus: 0.01 to 0.02 micrograms/kg/minute (10-20 nanograms/kg/min).1, 2 For persistent pulmonary hypertension of the newborn (PPHN): 0.01 to 0.05 micrograms/kg/minute (10-50 nanograms/kg/min).2

Answer 89

C. Left heart failure causing PulmHTN Normal PAPs/d is 25/7. This would be classed as severe (55) - (if image is correct) PAWP >15 means ‘ post-capillary’ cause or combined pre- and post. This is either group 2 or 5. A PVR might help differentiate. All other options (group 1,3,4 and 5) would likely have a isolated ‘pre-capillary’ PAWP of <15 LITFL and blue book 2015 article

Answer 90

B peak of T wave Triggering of the IABP is usually set according to the patient’s ECG tracing. When an R wave is detected the balloon is triggered to automatically start inflating in the middle of the T wave. Triggering can be impaired if the patient develops an arrhythmia, is paced or has a poor ECG trace. LITFL

Answer 91

b) VV ECMO VV ECMO Disadvantages - no cardiac support - local recirculation though oxygenator at high flows - reverse gas exchange in lung if FiO2 low - limited power to create high systemic arterial oxygen tension

Answer 92

b) 2 - if male CHA2DS2-VASc score ≥2 to be recommended chronic OAC (Grade 1A). - if female CHA2DS2-VASc score ≥3 to be recommended chronic OAC (Grade 1A). * non-sex risk factor also holds bearing: - For patients with CHA2DS2-VASc score of 1 in males and 2 in females based on age 65 to 74 years, we recommend chronic OAC (Grade 1A). Up to date: Our approach to deciding whether to prescribe anticoagulant therapy for patients with AF (excluding those with rheumatic mitral stenosis that is severe or clinically significant [mitral valve area ≤1.5 cm2], a bioprosthetic valve [surgical or bioprosthetic] within the first three to six months after implantation, or a mechanical heart valve) is as follows: *For a CHA2DS2-VASc score ≥2 in males or ≥3 in females, we recommend chronic OAC (Grade 1A). *For a CHA2DS2-VASc score of 1 in males and 2 in females: -For patients with CHA2DS2-VASc score of 1 in males and 2 in females based on age 65 to 74 years, we recommend chronic OAC (Grade 1A). Age 65 to 74 years is a stronger risk factor than the other factors conferring one CHA2DS2-VASc score point. -For patients with other risk factors, the decision to anticoagulate is based upon the specific nonsex risk factor and the burden of AF. For patients with very low burden of AF (eg, AF that is well documented as limited to an isolated episode that may have been due to a reversible cause such as recent surgery, heavy alcohol ingestion, or sleep deprivation), it may be reasonable to forgo chronic OAC and institute close surveillance for recurrent AF, although it may not be possible to reliably estimate AF burden from surveying symptoms or infrequent monitoring. The frequency and duration of AF episodes vary widely over time, and episodes are often asymptomatic. *For patients with a CHA2DS2-VASc of 0 in males or 1 in females, we suggest against OAC (Grade 2C). Patient values and preferences may impact the decision. For example, a patient who is particularly stroke averse and is not at increased risk for bleeding may reasonably choose anticoagulation, particularly if the patient is a candidate for treatment with a direct oral anticoagulant (DOAC). 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline

Answer 93

d) pregnancy A third heart sound reflects rapid left ventricular distention along with an increased atrioventricular flow Heard in Congestive heart failure Associated with Dilated Cardiomyopathy with dilated ventricles Less commonly valvular regurgitation and left to right shunts May be normal physiological finding in patients less than 40yrs old

Answer 94

d) No difference no observed beneficial effect of sevoflurane on the composite endpoint of prolonged ICU stay, mortality, or both in patients undergoing high-risk cardiac surgery

Answer 95

B. 50J ? In internal defibrillation, an initial dose of 20 joules is recommended to avoid burn-like injury to the myocardium. Care should be taken to avoid coronary vessels to prevent vessel damage. Subsequent doses can be increased to a maximum of 40 joules. Sterile internal pads must be used for internal defibrillation and should be readily available during any thoracotomy procedures Manufacturing manual for internal definition paddles say 50J maximum as higher has been shown to be damaging ## Footnote https://www.ncbi.nlm.nih.gov/books/NBK499899/

Answer 96

a. Tricuspid regurg Regurgitant CV waves: tricuspid regurgitation In tricuspid regurgitation, the backflow of blood out of the right ventricle obliterates the normal x descent. The c wave becomes accentuated and fuses with the v wave, as both are the results of right ventricular contraction (and the v wave peak pressure is often the same as the right ventricular peak systolic pressure). the reality is that they usually fuse completely to produce huge mutant waves, as seen here:

Answer 97

a) -30 Normal Axis https://litfl.com/super-axis-man-sam/ LITFL

Answer 98

a) Pulsus paradoxus electric 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. Physical findings of sinus tachycardia and the absence of frank hypotension may indicate significant hemodynamic compromise from cardiac tamponade and serve as an indication for immediate pericardiocentesis. In contrast, Kussmaul sign (the absence of an inspiratory decline in jugular venous pressure) is not usually seen in cardiac tamponade. Tachycardia and hypotension - Sinus tachycardia is seen in almost all patients, in an attempt to maintain cardiac output - Hypotension is somewhat more variably present - One exception is when the underlying disease is associated with bradycardia, as with a pericardial effusion and subacute cardiac tamponade associated with hypothyroidism. - Tachycardia also may not be seen in patients with early cardiac tamponade even though they have signs of a hemodynamically significant effusion, such as an elevated jugular venous pressure. Elevated jugular venous pressure - The JVP is almost always elevated in cardiac tamponade and may be associated with venous distension in the forehead and scalp. - CVP wave form: ->x descent is preserved ->y descent is attenuated or absent (due to the limited or absent late diastolic filling of the ventricle) Pulsus paradoxus -defined as: abnormally large decrease in systolic blood pressure (>10 mmHg) on inspiration - common finding in moderate to severe cardiac tamponade and is the direct consequence of ventricular interdependence. - not all patients with cardiac tamponade have pulsus paradoxus (eg, those with chronic hypertension leading to elevated ventricular diastolic pressures or those with a co-existent atrial septal defect). Pericardial rub — A pericardial rub may be heard in patients with cardiac tamponade due to inflammatory pericarditis. Electrocardiography - ECG in cardiac tamponade typically shows sinus tachycardia and may also show low voltage. - If pericarditis is present, the ECG findings typical of that disorder are also seen. - Electrical alternans is characterized by beat-to-beat alterations in the QRS complex and, in some cases, other electrocardiographic waves that reflect the swinging of the heart in the pericardial fluid. - Electrical alternans is relatively specific but not very sensitive for cardiac tamponade; rarely, this phenomenon is seen with very large pericardial effusions alone. 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 Presence of a pericardial effusion on echocardiography with evidence of cardiac chamber collapse, flow variation, or dilation of the inferior vena cava is consistent with, and highly suggestive of, cardiac tamponade. However, the diagnosis of cardiac tamponade can only be confirmed by the hemodynamic and clinical response to pericardial fluid drainage.

Answer 99

c) 420 ms i.e. RR interval = 60 / HR; therefore RR interval is 60/60 = 1 420 / square root of 1 is 420ms From LITFL: The corrected QT interval (QTc) estimates the QT interval at a standard heart rate of 60 bpm QT: Time from the start of the Q wave to the end of the T wave Represents time taken for ventricular depolarisation and repolarisation, effectively the period of ventricular systole from ventricular isovolumetric contraction to isovolumetric relaxation The QT interval is inversely proportional to heart rate: The QT interval shortens at faster heart rates The QT interval lengthens at slower heart rates An abnormally prolonged QT is associated with an increased risk of ventricular arrhythmias, especially Torsades de Pointes Corrected QT interval (QTc) The corrected QT interval (QTc) estimates the QT interval at a standard heart rate of 60 bpm This allows comparison of QT values over time at different heart rates and improves detection of patients at increased risk of arrhythmias Bazett formula: QTC = QT / √ RR Note: The RR interval is given in seconds (RR interval = 60 / heart rate).

Answer 100

PAPi goes down in acute RVF - actually designed to prognosticate in acute MI E is the answer https://www.ahajournals.org/doi/10.1161/CIRCHEARTFAILURE.121.009085#:~:text=The%20pulmonary%20artery%20pulsatility%20index,left%20ventricular%20assist%20device%20implantation.

Answer 101

E) LV hypertrophy ECHO FINDINGS intimal flap TYPING (type A): aortic regurgitation (acute dilatation of the aortic root, aortic leaflet prolapse, dissection flap prolapse, pre-existing disease, e.g. bicuspid valve) pericardial effusion and/or tamponade regional wall motion abnormality heralding coronary artery occlusion DOPPLER identifies true and false lumen detect aortic branch occlusion/ dissection (absent flow) Source LITFL

Answer 102

C 3L/min LVOT area x VTI = SV 3cm2 x 10cm = 30ml SV x HR = CO 30 x 100 = 3000

Answer 103

Maximum P-wave corresponds to placement in the Cavo-atrial Junction (CAJ) Benefits of CAJ placement - furthest distance from "high risk" areas - Largest vein diameter - highest blood flow capacity - minimal risk for catheter migration and looping Too short placement: Increased risk of: - DVT - Phlebitis Too long placement: Increased risk of: - arrhythmias - tricuspid valve dysfunction atrial dysfunction ECG and corresponding anatomy: - Normal P-wave = upper vasculature prior to CAJ - Max P-wav= CAJ - Initial negative P-wave deflection = Right Atrium - Biphasic P-wave = Right Atrium - Inverted P-wave = Right Ventricle

Answer 104

c. 90 Warm ischaemia time: - Time from treatment withdrawal to the start of cold perfusion of the donated organs - Significance is the impact on graft function - Most important phase of WIT begins when the systolic BP is < 60mmHg - This includes the waiting period from the absence of circulation to the declaration of death and the time before initiating the flow of cold perfusate through the cannula Maximum WARM Ischaemia time - Heart 30 mins - Liver 30 mins - Pancreas 30 mins - Kidney 60 mins - Lungs 90 mins Maximum COLD Ischaemia time: - Heart = 4 hrs - Lungs = 6-8hrs - Liver/Pancreas = 12hrs (DBD)/6 hrs (DCD) - Kidneys = 18hrs (DBD)/ 12 hrs (DCD)

Answer 105

Left heart failure (pulmonary htn with raised Left sided pressure (PCWP 24mmHg) PCWP >15mmHg. Therefore post-capillary or combined pre-and post-capillary PH = Left heart failure (clinical group 2) Other Options are clinical groups 1,3,4 of PH and therefore not correct (as characteristic is PAWP<15mmHg). WHO pulmonary Htn classification 1: Primary arterial Hypertension 2: 2ry to left heart disease 3: 2ry to lung disease/hyypoxia 4: Chronic Thromboembolic disease 5: Unclear/multifactorial

Answer 106

d) Peak of R wave The appropriate energy level is then selected, and the discharge/shock button is pressed and held. The defibrillator does not release the shock immediately. Instead, it waits for the next R-wave to appear and delivers the shock at the time of the R-wave. This allows the shock to be provided safely away from the T wave, avoiding the R-on-T phenomenon.

Answer 107

D) WPW B Sinus rhythm with very short PR interval (< 120 ms) Broad QRS complexes with a slurred upstroke to the QRS complexes — the delta wave Dominant S wave in V1 indicates a right-sided accessory path — sometimes referred to as “Type B” WPW Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of left ventricular hypertrophy (LVH) — again, this is due to WPW and does not indicate underlying LVH

Answer 108

Answer: A Aortic regurgitation - lack of dichrotic notch, high pulse pressure https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.111.060319#d1e195

Answer 109

c. Dobutamine In 2017 a similar questions was asked and an option for metaraminol was given, metaraminol could be a better answer as it will increase systemic pressure and reduce heart rate maintaining RCA perfusion at induction. Dobutamine and Milrinone can cause systemic vasodilation leading to reduction in systemic blood pressure and RCA perfusion pressure, Both adrenaline and Dopamine do not cause pulmonary vasodilation and can lead to tachyarhythmias Pulmonary hypertension and its management in patients undergoing non-cardiac surgery https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.12831 Vasoconstrictors, inotropes and inodilators Maintaining the gradient between aorta and right ventricle is achieved by using sympathomimetic and non-sympathomimetic vasopressors. Noradrenaline and vasopressin improve perfusion of the right coronary artery, reduce the pulmonary/systemic vascular resistance ratio, enhance right ventricular performance and marginally improve cardiac output However, the evidence of their impact on mortality related to right heart failure is weak. Inotropes that enhance right ventricular performance, such as adrenaline, dobutamine and levosimendan are effective in treating right-sided heart failure. The use of inotropes has a modest impact in reducing the overall mortality related to PH, and their wide availability and ease of administration make this group of drugs very attractive for use in the peri-operative setting. Inodilators, such as the phosphodiesterase-3 inhibitors milrinone and enoximone, have been shown to be beneficial when compared with conventional inotropic support only. It appears that the influence of phosphodiesterase-3 inhibitors on reducing pulmonary vascular resistance is more pronounced than the reduction in systemic vascular resistance. However, reduction in systemic vascular resistance can compromise right coronary artery blood flow in patients with severe PH and therefore they should be administered cautiously. Treatment of pulmonary hypertensive crisis: General principles - Avoid hypoxic pulmonary vasoconstriction - Avoid hypercarbia, acidosis and hypothermia - Avoid high airway pressures - Optimise right ventricular preload - Reduce right ventricular afterload - Maintain coronary blood flow - Maintain sinus rhythm - Maintain arterial blood pressure and cardiac output Vasopressors– noradrenaline; vasopressin Inotropes– adrenaline; dobutamine Inodilators– milrinone; enoximone Intravenous vasodilators (caution if low systolic blood pressure) - Milrinone (25–50 μg.kg−1 bolus, followed by 0.5–0.75 μg.kg−1.min−1 continuous infusion) - Prostacyclin (4–10 ng.kg−1.min−1 continuous infusion) - Iloprost (1–3 ng.kg−1.min−1 continuous infusion) - Sildenafil (10 mg bolus three times a day) Selective pulmonary vasodilation - Iloprost (5–10 μg diluted in 10 ml saline, nebulised over 10 min, repeated every 2–4 h) - Prostacyclin (25–50 μg diluted in 50 ml saline, nebulised over 15 min, repeated every hour) - Nitric oxide (5–40 ppm continuously)

Answer 110

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 ## Footnote https://pubs.asahq.org/anesthesiology/article/121/5/914/13855/VasopressinThe-Perioperative-Gift-that-Keeps-on

Answer 111

EXCEPT C) RV dilation Echo findings in Aortic Dissection: 1. Intimal flap 2. Type A dissection: - Aortic regurgitation -Acute dilation of aortic root -Aortic leaflet prolapse -Dissection flap prolapse -Pre-existing disease -Pericardial Effusion/Tamponade -RWMA 3. Colour flow doppler -identifies true and false lumen -aortic branch occlusion/dissection

Answer 112

e) sinus tachycardia https://academic.oup.com/bjaed/article/9/2/61/299563 Typically anorexic patients are hypotensive and bradycardic. Bradycardia reflects the decrease in basal metabolic rate that arises as an adaptive response to starvation Electrocardiographic abnormalities are common and may be found in >80% of strict dieters. These include: 1. atrioventricular block 2. ST depression 3. T wave inversion 4. QT prolongation.

Answer 113

B. distal to LSCA The appropriate performance of the IABP is dependent on proper position. Ideally, the tip of the balloon should be positioned 2–3 cm distal to the origin of the left subclavian artery (LSCA) ## Footnote https://academic.oup.com/bja/article/110/2/316/228037

Answer 114

c) Pleural effusion Source: BJA Ultrasound in critical care Thoracic US revealing a large pleural effusion (E) that has displaced the lung. The diaphragm (D) and liver (L) are visualized. The depth from the skin to the fluid has been measured. Insertion of the needle at this site is not advised; given the proximity to the liver, a more superior approach should be marked.

Answer 115

RCA (Inferior STEMI) - 80% RCA - 18% LCx - 2% rare wrap around LAD ST elevation in lead III > lead II Presence of reciprocal ST depression in lead I Signs of right ventricular infarction: STE in V1 and V4R Source LITFL

Answer 116

A - Modified WHO class 4 B - Modified WHO class 3 (4 if ANY complication) C - Modified WHO class 2-3 (if severe AS - 4) D - Modified WHO class 1 Class 4 = 40-100% risk of event Source https://academic.oup.com/eurheartj/article/39/34/3165/5078465 Table: https://academic.oup.com/view-large/186437995

Answer 117

E LAFB: > Left axis deviation (usually -45 to -90 degrees) > qR complexes in leads I, aVL > rS complexes in leads II, III, aVF > Prolonged R wave peak time in aVL > 45ms LPFB: > Right axis deviation (RAD) (> +90 degrees) > rS complexes in leads I and aVL > qR complexes in leads II, III and aVF > Prolonged R wave peak time in aVF

Answer 118

c. Long E time Spont vent not appropriate for this surgery as will require RSI so spont vent can't be ensured 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

Answer 119

C. No Anticoagulation - if male CHA2DS2-VASc score ≥2 to be recommended chronic OAC (Grade 1A). - if female CHA2DS2-VASc score ≥3 to be recommended chronic OAC (Grade 1A). * non-sex risk factor also holds bearing: - For patients with CHA2DS2-VASc score of 1 in males and 2 in females based on age 65 to 74 years, we recommend chronic OAC (Grade 1A). Up to date: Our approach to deciding whether to prescribe anticoagulant therapy for patients with AF (excluding those with rheumatic mitral stenosis that is severe or clinically significant [mitral valve area ≤1.5 cm2], a bioprosthetic valve [surgical or bioprosthetic] within the first three to six months after implantation, or a mechanical heart valve) is as follows: *For a CHA2DS2-VASc score ≥2 in males or ≥3 in females, we recommend chronic OAC (Grade 1A). *For a CHA2DS2-VASc score of 1 in males and 2 in females: -For patients with CHA2DS2-VASc score of 1 in males and 2 in females based on age 65 to 74 years, we recommend chronic OAC (Grade 1A). Age 65 to 74 years is a stronger risk factor than the other factors conferring one CHA2DS2-VASc score point. -For patients with other risk factors, the decision to anticoagulate is based upon the specific nonsex risk factor and the burden of AF. For patients with very low burden of AF (eg, AF that is well documented as limited to an isolated episode that may have been due to a reversible cause such as recent surgery, heavy alcohol ingestion, or sleep deprivation), it may be reasonable to forgo chronic OAC and institute close surveillance for recurrent AF, although it may not be possible to reliably estimate AF burden from surveying symptoms or infrequent monitoring. The frequency and duration of AF episodes vary widely over time, and episodes are often asymptomatic. *For patients with a CHA2DS2-VASc of 0 in males or 1 in females, we suggest against OAC (Grade 2C). Patient values and preferences may impact the decision. For example, a patient who is particularly stroke averse and is not at increased risk for bleeding may reasonably choose anticoagulation, particularly if the patient is a candidate for treatment with a direct oral anticoagulant (DOAC). 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline

Answer 120

Adenosine (effect is exagerated)

Answer 121

c. Late inflation

Answer 122

b) pulmonary trunk

Answer 123

d. Cardiac tamponade Deranged physiology In summary The CVP is raised All CVP waveform components are elevated a and v waves are tall x descent is steep y descent is (usually) absent

Answer 124

First degree heart block + Left Anterior hemiblock ECG criteria for LAFB/LAHB Left axis deviation (usually -45 to -90 degrees) qR complexes in leads I, aVL rS complexes in leads II, III, aVF Prolonged R wave peak time in aVL > 45ms

Answer 125

c. sinus tachy with prolonged QRS

Answer 126

d) VT https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

Answer 127

a) No increased risk of bleeding There is no evidence that pre-operative aspirin administration resulted in a lower risk of death or thrombotic complications, or a higher risk of haemorrhage. The study aim (and title) was to compare stopping vs continuing aspirin, however the design insisted on all patients stopping aspirin and then being given a single dose of aspirin or placebo prior to surgery (and presumably all patients were given aspirin after surgery) – this method hasn’t really investigated the theory TheBottomLine.org.uk

Answer 128

C- Multifocal Atrial Tachycardia Cardioversion is contraindicated in MAT. Due to the multiple atrial foci, direct current (DC) cardioversion is not effective in restoring normal sinus rhythm and can precipitate more dangerous arrhythmias. - https://emedicine.medscape.com/article/155825-overview#a10 DCCV is indicated for 1. Any haemodynamically unstable narrow or wide QRS complex tachycardia 2. AF <48hrs 3. AF >48hrs with adequate anticoag/TOE to exclude thrombus 4. SVTs and monomorphic TVs not responding to trial of IV medical therapy DCCV is CONTRAindicated in: a. Digitalis toxicity and associated tachycardia b. AF >48hrs without adequate anticoagulation/TOE -BJAEducation 2017 https://academic.oup.com/bjaed/article/17/5/166/2669966

Answer 129

d) Atropine Blue book 2019

Answer 130

New question. a) 30 day mortality Postoperative myocardial injury was associated with an increased risk of death. Twenty-seven of the 315 patients (8.6%; 95% CI, 6.0–12.2%) with myocardial injury died within 30 days compared with 29 of the 1312 patients (2.2%; 95% CI, 1.5–3.2%) with normal troponin I levels (P<0.01) Reference: Myocardial Injury After Noncardiac Surgery and its Association With Short-Term Mortality (Circulation 2013)

Answer 131

A) Type 1 MI Clinical classification based on the assumed proximate cause of the MI: - Type 1 ○ MI caused by atherothrombotic coronary artery disease ○ And usually precipitated by atherosclerotic plaque disruption ( rupture or erosion) - Type 2 ○ MI consequent to a mismatch between oxygen supply and demand ○ Multiple potentional mechanisms: § Coronary dissection § Vasospasm § Emboli § Microvascular dysfunction § Increases in demand without underlying coronary artery disease - Type 3 ○ Patient with typical presentation of MI (ECG changes or VF) with unexpected death before blood samples for biomarkers could be drawn - Type 4a ○ MI associated with Percutaneous Coronary intervion (PCI) - Type 4b ○ Subcategory of PCI related MI related to stent/scaffold thrombosis - Type 5 CABG related MI

Answer 132

c) falsly low SpO2 Effects of hihg dose hydroxycobalamin: - red urine - thrombocytosis - leukopenia

Answer 133

D> Myocardial ischaemia An inverted U wave may represent myocardial ischemia (and especially appears to have a high positive predictive accuracy for left anterior descending coronary artery disease[7] ) or left ventricular volume overload. ^Wikipedia -------- U-wave inversion is abnormal (in leads with upright T waves) A negative U wave is highly specific for the presence of heart disease Common causes of inverted U waves Coronary artery disease Hypertension Valvular heart disease Congenital heart disease Cardiomyopathy Hyperthyroidism In patients presenting with chest pain, inverted U waves: Are a very specific sign of myocardial ischaemia May be the earliest marker of unstable angina and evolving myocardial infarction Have been shown to predict a ≥ 75% stenosis of the LAD / LMCA and the presence of left ventricular dysfunction ^LITFL: https://litfl.com/u-wave-ecg-library/

Answer 134

D) Mitral Stenosis (Rheumatic, moderate to severe) DOAC use is contraindicated in certain clinical conditions, notably, in patients who have a mechanical heart valve and those with rheumatic mitral stenosis. Moderate to severe renal impairment or significant hepatic disease is also a contraindication to DOAC treatment Bioprosthetic valves are less thrombogenic thus DOAC use is acceptable. https://www.ahajournals.org/doi/epdf/10.1161/JAHA.120.017559

Answer 135

e. peak of R wave https://derangedphysiology.com/main/required-reading/cardiothoracic-intensive-care/Chapter%20634/normal-iabp-waveform https://litfl.com/intra-aortic-balloon-pump-trouble-shooting/

Answer 136

a) Tamponade Cardiac tamponade occurs ~1%. Can usually be managed with reversal of anticoagulation and percutaneous drainage. Vascular complications most common followed by tamponade. https://www.ahajournals.org/doi/10.1161/circep.113.000768 https://academic.oup.com/bjaed/article/12/5/230/289246#3659733

Answer 137

d) Dexamethasone The ECG shows LONG QT https://litfl.com/qt-interval-ecg-library/

Cardiac surgery and interventional cardiology Flashcards

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