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146 Cards in this Set
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TMP-Mar11-032
[Aug12] 75 year old with non-valvular AF usually on warfarin has their warfarin stopped for one week. What is their daily risk of stroke? A: 1% B: 0.1% C: 0.01% D: 4% E: 10% |
C 0.01%
-- CHADS2 (CCF, Hypertension, Age ≥75 years, DM, Stroke/TIA or Thromboembolism) - pts score would be 1 which gives annual stroke risk of 2.8% - does that translate to a daily stroke risk of ~0.01% ? CHA2DS2-VASc (CCF, HT, Age ≥75 years, DM, Stroke/Tia or thromboembolism, Vascular disease (IHD, PVD etc), Age 65-74, Sex category (female)) - pts score would be 3 - scores 2 for being 75 - so his annual stroke risk would be 2.2% ----------- |
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TMP-Sep11-082 [Mar12][Aug12]
Atrial Septal Defect (ASD) murmur is due to flow through which valve? A. ASD B. Tricuspid valve C. Pulmonary valve D. Mitral valve E. Aortic valve |
C. Pulmonary valve
(where is the ASD spot?) -- From Talley O'Connor 5th ed. ASD: - Ostia secundum (90%) where defect does not involve AV valves and ostia primum where defect involves AV valves - Auscultation: fixed splitting of S2, defect produces no direct murmur but increased flow through R side of heart can produce low pitched diastolic tricuspid flow murmur and more often a pulmonary systolic ejection murmur louder on inspiration. - From emedicine: - Findings on examination depend on degree of L-R shunt and hemodynamic consequences. - Hyperdynamic RV impulse due to increased diastolic filling and stroke volume. - Palpable pulsation of PA and ejection click can be detected because of a dilated pulmonary artery - S1 is typically split and second component may be increased in intensity due to forceful RV contraction and delayed closure of TV - S2 is often widely split and fixed due to reduced respiratory variation from delayed PV closure (only seen if PAP is normal and PVR is low). This is the CHARACTERISTIC abnormality found in almost ALL pts with large L-R shunts. - blood flow across ASD does not cause a murmur at site of shunt because no substantial pressure gradient exists between the atria. - however ASD with moderate-large L-R shunts -> pulmonary systolic ejection murmur (crescendo-decrescendo) due to increased stroke volume rather than any valvular problems. - large L-R shunts often have rumbling mid diastolic murmur at TV because of increased flow. Auscultatory findings may resemble those of mild valvular or infundibular pulmonic stenosis and idiopathic dilation of pulmonary artery. - these all produce a systolic ejection murmur but DIFFER from ASD by movement of S2 with respiration, a pulmonary ejection click or absence of a tricuspid flow murmur. ----------- |
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Child with murmur- what would make it more likely for you to investigate if you heard the murmur
A. persist in supine position B. louder or softer with various manouveres |
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TMP-Sep11-053
(similar to MC135) During cardiac catheterisation (?) patient become BP 80/60, HR 110, CVP 16. What is the next most important investigation A. Echocardiogram B. CXR C. Electrocardiogram |
A
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TMP-Mar11-039
See also MC157 Fontan patient having an open appendicectomy. What do you want? A: long I time and PEEP B: long I time C: short I time D: raised ETCO2 E: spontaneous ventilation |
C: short I time
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In Eisenmengers it is NOT true that
A. An important goal is to maintain the shunt, by minimising changes to SVR and PVR B. High Hb should be maintained C. A gaseous induction is an effective method that avoids CVS compromise D. If GA is required then ketamine is the drug of choice E. Careful attention to IV infusions is needed to prevent air entrainment and paradoxical emboli |
C. A gaseous induction is an effective method that avoids CVS compromise
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MC03 ANZCA version [Aug04][Apr05][Apr08]
What percent of patients have a probe-patent foramen ovale? A. 0-10% B. 10-20% C. 20-35% D. 30-40% E. 40-50% |
C. 20-35%
Ref 1: Stoelting, Anaesthesia and Co-Existant Disease p46-"30% of normal patients...FO remains probe patent" Ref 2: Kaplan, Cardiac Anaesthesia p685-"probe patency of FO... in 25% of individuals over 20 years of age" from Nabil Saleh (Nov 2001) ----------- |
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MC03b ANZCA version [2002-Mar] Q79, [2002-Aug] Q30
An INCORRECT statement regarding patent foramen ovale (PFO) in adults is that: A. it is found in 5% of patients at postmortem examination B. it can cause hypoxaemia C. it is best seen using transoesphageal echocardiography D. an asymptomatic PFO requires no intervention E. the sitting position should be avoided in patients with a PFO |
A. it is found in 5% of patients at postmortem examination
30% have a probe patent PFO on autopsy, and in vivo, 20% can detect on sensitive tests e.g colour Doppler ~~ B. it can cause hypoxaemia – TRUE - via many mechanisms, mainly shunt if significant C. it is best seen using transoesphageal echocardiography – TRUE, especially with a bubble test D. an asymptomatic PFO requires no intervention – TRUE – just caution E. the sitting position should be avoided in patients with a PFO – TRUE - 14% paradoxical air embolism rate ----------- Sitting Position Anesthesiology: Volume 93(4) October 2000 pp 971-975 MANY neurosurgeons prefer the sitting position for neurosurgical procedures in the posterior fossa and in the cervical spine because it provides optimum access to midline lesions, improve cerebral venous drainage, lowers intracranial pressure, and promotes gravity drainage of blood and cerebrospinal fluid. However, during procedures in the sitting position, venous air embolism (VAE) has been reported to occur in 23-45% of the patients, depending on the type of operation and the monitoring method used. VAE can cause a paradoxical air embolism in the presence of a right-to-left shunt, of a patent foramen ovale (PFO), and probably also by transpulmonary passage. Increases in pulmonary vascular resistance and right atrial pressure will predispose to paradoxical air embolism if VAE occurs. Paradoxical air embolism has been reported to occur in 14% of neurosurgical patients undergoing surgery in the sitting position and may result in serious, possibly fatal, coronary and cerebral ischemic complications. PFO notes Natural interatrial channel, limited inferiorly by the flap like septum primum, and superiorly by the thicker septum secundum. At birth with pressure reversal, the septum primum is forced closed by left atrial pressure to close the foramen ovale. Fusion normally occurs by means of fragile fibrous adhesions in the first years of childhood, but when this does not occur, an oblique tunnel like opening persists between the septa, known as PFO. This differs from an ASD which is not a valve like structure, but rather a true defect in the septum. PFO usually allows right to left shunting, but can allow left to right, despite its valve like nature. RLS through a PFO may occur under several sets of physiological conditions including valsalva. Valsalva causes a transient rise in right atrial pressure above the left atrial pressure, reversing the interatrial pressure gradient, with resultant RLS across the PFO. In a substantial number of persons, the foramen ovale stays patent throughout life. Autopsy studies performed on adolescents and adults have found an overall incidence of 27%, but this varies with age, from a mean of 35% before 30 years to 22-27% at 30-90 years (Thompson & Evans 1930, Patten 1931, Hagen et al. 1984). Neither the incidence of PFO nor its size varies between the sexes. One study has suggested familial aggregation of PFO (Arquizan et al. 2001). PFO cannot be identified by history, physical examination or chest x-ray. TTE is widely available, but is less sensitive than TEE, which is currently regarded as the gold standard for the detection of PFO (Hausmann et al. 1992, Belkin et al. 1994). As a PFO is not a discontinuity in the septum but a valve-like structure, intravenous administration of echo contrast material is usually required to detect RLS. Commonly used contrast agents include air-saline microbubbles, or galactose or oxypolygelatin suspensions. Diseases linked to PFO include: Ischaemic stroke – significant association of PFO with iscaemic stroke in general, and especially cryptogenic stroke in patients younger than 55 Pulmonary embolism – if also has PFO, associated with significant hypoxaemia and cerebral/peripheral ischaemic events. COPD – higher incidence of PFO in severe COPD OSA – incr prevalence of PFO Gas embolism Fat embolism Platypnoea-orthodeoxia syndrome – rare syndrome of dyspnoea induced by assuming an upright position, relieved in supine position. Migraine Transient global amnesia Paradoxical embolism to other organs |
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MC05
A twenty-year-old woman undergoes cardiac catheterization for fatigue, cyanosis and a loud systolic murmur over the left second inter-costal space anteriorly. Chest x-ray reveals right ventricular hypertrophy. The cardiac catheter shows a large atrial septal defect. The cardiac catheterization result which is most likely to predict problems separating from cardiopulmonary bypass is an elevated A. pulmonary artery pressure B. left ventricular end-diastolic pressure C. pulmonary wedge pressure D. pulmonary vascular resistance E. right ventricular pressure |
D. pulmonary vascular resistance
She has an ASD. If PVR is very high, then it may be irreversible and the heart may have been surviving on the R->L shunt, thus ASD repair may cause Rt failure. PAP will be high even in early ASD due to extra blood flow. (pjs) ~~ ASD Accounts for 9% of all congenital heart defects (2nd most common) More common in females 2-3:1 Secundum ASDs are most common (75%) Often associated with mitral valve abnormalities Occur because of spontaneous genetic mutations Shunt likely to occur if ASD > 2cm in diameter – increased pulmonary blood flow Surgical correction required when PBF > 1.5 x SBF Signs and symptoms include: dyspnoea on exertion, SVT, RHF, paradoxical embolism, pulmonary infections, RAD, RBBB, AF Anaesthetic management, avoid increases in SVR, and large decreases in PVR, which promotes LRS. Volatiles and IPPV tend to decrease SVR and increase PVR which is good. ----------- Paediatric Cardiology for Practitioners Myung K. Park p 417 – Pressure is related to both flow and vascular resistance. An increase in flow, vascular resistance or both can result in pulmonary hypertension. Regardless of its cause, pulmonary hypertension eventually involves constriction of the pulmonary arterioles, resulting in an increase in pulmonary vascular resistance and hypertrophy of the RV (cor pulmonale). The right ventricle cannot sustain sudden pressure loads over 40 – 50 mmHg. P133 Re: ASD. Mortality. Fewer than 1% of patients die; however, there is a greater risk for small infants and those with increased pulmonary vascular resistance. Increased pulmonary blood flow increases the pulmonary artery pressure. Pulmonary vascular resistance gradually increases. When PVR increases, right ventricular hypertrophy develops with a further increase in pulmonary pressures, and a decrease in the volume of the left-to-right shunt. Eventual equalization of ventricular pressures occurs with bi-directional shunting and finally, with severe pulmonary vascular hypertension, the shunt reverses to a right to left pattern leading to cyanosis. The cyanotic phase of this process is called the Eisenmenger syndrome and is usually considered inoperable (need heart-lung transplant) Surgical closure of septal defects is intended to halt this progression. In patients with elevated PA pressures, the increased PVR may be primarily flow dependent and hence, reversible by surgical therapy. In patients with fixed (irreversible) PVR, however, closure of the defect may precipitate acute right heart failure and death. http://indianheartjournal.com/SeptOctober2001/abstact/659-662/267_noninvasive.htm Estimation of PO2 at rest and after exercise, bidirectional color flow across the ASD and absence or paradoxical septal motion best predict elevation in PVRI to inoperable levels in patients with ASD. |
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MC19
Tall R wave in V1 indicates: A. RBBB B. Posterior MI C. WPW syndrome D. RV hypertrophy |
All of the above
~~ Tall R wave in V1 • Posterior MI • RBBB • RVH • WPW • Misplaced electrode • Dextrocardia ----------- A. RBBB – RSR in V1 B. Posterior MI – tall R waves anteriorly and ST depression anteriorly indicate q waves posteriorly and ST elevation. None of the standard leads look at the posterior wall, which thus needs to be viewed indirectly. C. WPW syndrome – Type A only. delta wave in absence of q wave ---- THE TALL R WAVE IN LEAD V1 Under normal circumstances, the QRS complex in lead V1 is predominantly negative. Finding a "Tall" R wave in lead V1 (i.e., an R wave that equals or exceeds the S wave in this lead) is distinctly unusual & should prompt consideration of the following: Common Causes of a Tall R Wave in Lead V1 (#s correspond to diagram - see picture): 1. WPW • QRS widening & short PR interval. • Delta waves (which may be positive or negative). 2. RBBB • QRS widening to > .11 second. • RSR' (or RBBB equivalent pattern) in lead V1. • Wide, terminal S wave in leads I and V6. 3. RVH • Normal QRS duration & RAA (right atrial abnormality) diagnosed by the finding of tall Peaked and Pointed P waves in the Pulmonary leads (II, III, aVF). If the P wave looks "uncomfortable to sit on", think RAA!!! • RAD or indeterminate axis/Low voltage. • Persistent precordial S waves. 4. Right ventricular strain. • Posterior Infarction -Normal QRS duration • Evidence of inferior infarction • Positive "mirror test" 5. Normal Variant • Normal QRS duration • Diagnosed by exclusion (i.e., after ruling out WPW, RBBB, RVH, & posterior infarction) • Often found in otherwise healthy young adult |
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MC19b ANZCA Version [Jul06] Q17, [Apr07]
A 50 year old patient is admitted with acute chest pain. An ECG shows tall R waves in lead V1. The most likely diagnosis is A. occlusion of the anterior descending coronary artery B. a lateral myocardial infarction C. pulmonary infarction D. posterior myocardial infarction E. occlusion of the circumflex artery |
D. posterior myocardial infarction - true:
"Tall lead V1 (tall RV1), defined as an R/S ratio equal to or greater than 1, is not an infrequent occurrence in emergency department patients. This electrocardiographic finding exists as a normal variant in only 1% of patients. Physicians should therefore be familiar with the differential diagnosis for this important QRS configuration. The electrocardiographic entities which can present with this finding include right bundle branch block, left ventricular ectopy, right ventricular hypertrophy, acute right ventricular dilation (acute right heart strain), type a Wolff-Parkinson-White syndrome, posterior myocardial infarction, hypertrophic cardiomyopathy, progressive muscular dystrophy, dextrocardia, misplaced precordial leads, and normal variant." C. and E. can also have R in V1 but D. is most likely ----------- |
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MC20b [Apr08][Oct08]
Electrocardiographic changes in acute hyperkalaemia include A. the appearance of a J wave B. loss of P waves C. flattening of the T wave D. a prominent U wave E. a prolonged QT interval |
B. loss of P waves
➮ Wide, flat or absent P waves ➮ Prolonged PR ➮ Widened QRS ➮ Tall peaked T waves (earliest change) ➮ S-T segment depression ➮ Ventricular arrhythmias ➟ tachycardias and fibrillation ➮ Asystole Hyperkalaemia ➮ 5.5-6.0 - Mild ➮ 6.1-7.0 - Moderate ➮ > 7.0 - Severe ----------- |
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MC22
Fourth heart sound: A. Rapid filling in atrial diastole B. Low pitched ound C. Normally present D. Due to atrial contraction E. Due to rapid emptying of atrium in early diastole |
D. Due to atrial contraction
Due to a high pressure atrial wave reflected back from a poorly compliant ventricle e.g. aortic stenosis, hypertensive heart disease OHCM160 a- STIFF – wall – late diastolic dysfunction? A. Rapid filling in atrial diastole – No, its the 3rd heart sound is rapid ventricular filling during diastole – SLOSH- ing in B. Low pitched sound – NO S3 is low pitched, and best heard by bell. S4 is usually higher pitched C. Normally present – NO always ABnormal, but S3 can be normal in young people E. Due to rapid emptying of atrium in early diastole – NO - atrium empties late in diastole (atrial kick) ----------- |
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MC28
The most important feature differentiating chronic liver disease and heart failure is: A. JVP raised B. Ascites C. Cirrhosis D. Peripheral oedema E. Hepatomegaly |
A. JVP raised
see wiki ----------- |
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MC30b ANZCA version [2004-Aug] Q128, [2005-Apr][Sep11]
A patient with pulmonary hypertension secondary to lung disease presents for a laparotomy. Regarding this patient's anaesthetic management A. an alpha-agonist is the inotrope of choice B. hypothermia is protective against rises in pulmonary artery pressure C. isoflurane will tend to decrease pulmonary artery pressure D. ketamine is an appropriate anaesthetic agent E. right heart failure is not a concern |
A. an alpha-agonist is the inotrope of choice
- A. an alpha-agonist is the inotrope of choice - probably true and best answer: there are No α-1 adrenergic receptors are present in the pulmonary circulation (Blaise, Anaesthesiology, 2003, 99(6):1421) so α-1 agonists are fine and may assist RV function by increasing coronary perfusion pressure (although some prefer dobutamine initially becuase it increases contractility and may pulmonary vasodilate) the wording is confusing and might subequently change now. Both the Blaise article and Stoelting 5th ed. suggest that causes of hypotension are multifactorial and should be treated accordingly. Specifically pulm HTN crisis requiring inotropy, the 'inotrope' of choice might be milrione (or possibly dobutamine), however R heart ischaemia and low SVR (with fixed PVR) are important causes of hypotension specifically treated with noradrenaline B. hypothermia is protective against rises in pulmonary artery pressure - false Hypothermia increases PVR (A & A ,Volume 96(6), June 2003, pp 1603-1616) C. isoflurane will tend to decrease pulmonary artery pressure - false PVR does not change with volatiles except N2O which does increase PVR (Stoelting Pharmacology p47) Isoflurane has no effect on baseline pulmonary vessel tone. (Blaise, Anaesthesiology, 2003, 99(6):1421) D. ketamine is an appropriate anaesthetic agent - false 'In patients who have pulmonary artery pressure, ketamine seems to cause a more pronounced increase in pulmonary than systemic vascular resistance' (Miller, p348) 'The sympathomimetic properties of ketamine may preclude use in the setting of pulmonary hypertension (Yao, p96) In-vitro ketamine increases PVR in rat lung...(and)...ketamine attenuates endothelium-dependent pulmonary vasorelaxation in response to acetylcholine and bradykinin ...(and)...sympathetic innervation of the pulmonary circulation does exist (Blaise, Anaesthesiology, 2003, 99(6):1421) E. right heart failure is not a concern - false ----------- |
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MC32
Which may be the only constant finding in pulmonary thromboembolism? A. Increased temperature B. Haemoptysis C. Tachypnoea D. Tachycardia E. Pleural pain F. Increased PCO2 G. Paradoxical splitting of second heart sound |
D. Tachycardia
(pjs - i think tachypnoea is a better answer see below) ~~ ----------- S&D p173 Clinical manifestations of pulmonary embolism are non-specific and the diagnosis is often difficult to establish on clinical grounds alone. The most consistent manifestations of pulmonary embolism are an acute onset of dyspnoea, which most likely reflects sudden increases in alveolar deadspace, and decreases in pulmonary compliance. Reflex bronchoconstriction augments airway resistance and lung oedema decreases pulmonary compliance Signs and symptoms of PE % incidence Acute dyspnoea 80-85 Tachypnoea (>20/min) 75-85 Pleuritic chest pain 65-70 Non-productive cough 50-60 Accentuation of P2 50-60 – due to elevation of pulmonary artery pressure. Wheeze 50-60 Tachycardia (>100/min) 45-65 Fever (38-39) 40-60 Haemoptysis 30 |
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MC34
What is the energy required to defibrillate a patient in AF using external chest electrodes? A. 10 Joules B. 40-75 J C. 250 J D. 400 J E. 750 J |
C. 250 J
From ACC/AHA guidelines 2006 exec summary: In 64 pts assinged to initial monophasic energies of 100/200/360J, high initial energies were assoc higher succes rates (14/ 39/ 95% respectively) resulting in fewer shocks and less cummulative energy. 100J is probably too low, hence 200J or greater is recommended. A similar recommendation to start with 200J applies to biphasic waveforms, partic when cardioverting patients with AF of long duration. ----------- |
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MC36
A 50 year old man presented with a myocardial infarction. His BP is 90/40, PCWP is 4 and he is oliguric. You would: A. Give Digoxin and diuretics B. Give vasodilators and decrease afterload C. Give Lasix (frusemide) which will vasodilate and cause diuresis D. Fluid load with albumin solution E. Sedate and relieve pain |
D. Fluid load with albumin solution
Low PCWP together with oliguria low implies he is hypovolaemic relatively, and not in acute LV failure. PCWP (Pulmonary Capillary Wedge Pressure) is an indirect indicator of left ventricular filling pressure or preload. Normal: 8-12mmHg ~~ A. – diuresis would worsen volume depletion B. Give vasodilators and decrease afterload – will bottom out pressure even more C. – frusemide is a venodilator, and is useful in failure due to relative fluid overload. E. Sedate and relieve pain – pain relief is important in MI, as it may reduce anxiety and reduce myocardial oxygen demand ----------- http://www.cvphysiology.com/Heart%20Failure/HF008.htm PULMONARY CAPILLARY WEDGE PRESSURE The measurement of pulmonary capillary wedge pressure (PCWP) provides an indirect measure of left atrial pressure and is particularly useful in the diagnosis of left ventricular failure and mitral valve disease. The measurement is made as follows. A balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) is advanced from a peripheral vein into the right atrium, the right ventricle, and then positioned within a branch of the pulmonary artery. There is one opening (port) at the tip of the catheter (distal to the balloon) and a second port several centimeters proximal to the balloon. These ports are connected to pressure transducers. When properly positioned in a branch of the pulmonary artery, the distal port measures pulmonary artery pressure (~ 30/15 mmHg) and the proximal port measures right atrial pressure (~ 0-2 mmHg). The balloon is then inflated with air using a syringe (the balloon volume is about 1 ml) and this occludes the branch of the pulmonary artery. When this occurs, the pressure in the distal port rapidly falls, and after about 10 seconds, reaches a stable lower value that is very similar to left atrial pressure (normally about 8-10 mmHg) – a continuous column of blood from the pulmonary vessel to the left atrium, which should be the same pressure. The balloon is then deflated. The recorded pressure during balloon inflation is similar to left atrial pressure because the occluded vessel, along with its distal branches which eventually form the pulmonary veins, acts as a long catheter which measures the blood pressures within the pulmonary veins (this pressure is virtually the same as mean left atrial pressure). A PCWP exceeding 15 mmHg suggests mitral stenosis, mitral insufficiency, severe aortic stenosis, aortic regurgitation, ventricular failure, or other cardiac defects or pathologies. When the PCWP exceeds 20 mmHg, the transmission of this pressure back into the pulmonary vasculature increases pulmonary capillary hydrostatic pressure which can lead to pulmonary congestion and edema. Pulmonary capillary wedge pressures are also useful in evaluating blood volume status when fluids are administered during hypotensive shock. One practice is to administer fluids at a rate that maintains PCWP between 12-14 mmHg. |
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MC38 [Aug12]
Causes of inverted P waves in Lead II of the electrocardiogram include A. transposed lower limb leads B. junctional rhythm C. hypothermia D. left axis deviation E. inferior myocardial infarction |
B. junctional rhythm
– retrograde activation of atria, originating from the a-v node - may also have smaller PR interval ~~ C. hypothermia – Osborn waves - a rounded hump at the J point D. left axis deviation – positive in 1, negative in aVF ----------- |
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MC39
A thirty year old male presents in cardiac failure with severe aortic incompetence. His blood pressure is 120/50 mmHg and pulmonary capillary wedge pressure is 30 mmHg. Which of the following forms of therapy is contraindicated? 1. dopamine infusion 2. sodium nitroprusside infusion 3. isoprenaline infusion 4. intra-aortic balloon counterpulsation |
4. intra-aortic balloon counterpulsation
– fast full and forward for a regurgitant lesion, implying that decreased SVR is the go, however this dude is in failure. SNP will achieve this, but will also drop BP. This probably doesn’t contraindicate its use. IABP INDICATIONS 1. Acute left ventricular failure 2. Cardiogenic shock 3. Unstable refractory angina 4. Impending myocardial infarction 5. Mechanical complications if acute MI, i.e. VSD, papillary muscle rupture 6. Ischaemia related, intractable ventricular arrhythmias 7. Cardiac support for high-risk angioplasty patients and general surgery patient. CONTRAINDICATIONS 1. Severe aortic insufficiency 2. Aortic aneurysm and dissecting aortic aneurysms 3. Coagulopathy 4. Severe calcific aorto-iliac disease or peripheral disease 5. Infection ----------- |
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MC42 ANZCA version [apr04][Mar11][Sep11][Aug12]
Abnormal Q waves are NOT a feature of the ECG in A. an old myocardial infarction B. left bundle branch block C. recent transmural myocardial infarction D. digitalis toxicity E. Wolff-Parkinson-White syndrome |
D. digitalis toxicity
Digoxin is associated with ST depression and other arrhythmias and calcium channel blockers with AV conduction disturbances. (harrison’s 1267-70) Q waves: transmural MI, LBBB, hyperkalaemia, WPW, amyloid, HOCM, cardiac contusion, myocarditis, dextrocardia, reverse limb leads. Epstein page 52. ----------- |
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MC49 ANZCA version [2001-Apr]
Inverted T waves in the ECG occur in 1. pericarditis 2. hypokalaemia 3. ventricular hypertrophy 4. cardiomyopathy |
1. pericarditis
Diff Dx T wave inversion Q wave and non-Q wave MI (e.g., evolving anteroseptal MI): Myocardial ischemia Subacute or old pericarditis Myocarditis Myocardial contusion (from trauma) CNS disease causing long QT interval (especially subarrachnoid *hemorrhage) Idiopathic apical hypertrophy (a rare form of hypertrophic cardiomyopathy) Mitral valve prolapse Digoxin effect RVH and LVH with "strain" ----------- |
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MC51 [Aug10]
The chief concern in the anaesthetic management of mitral stenosis is to avoid tachycardia because it: A. Increases the transmitral pressure gradient B. Aggravates left ventricular ischaemia C. Increases myocardial oxygen consumption D. Frequently precipitates atrial fibrillation E. Reduces the size of the left atrium |
A. Increases the transmitral pressure gradient
– normally less than 2 mmHg (higher in left atrium than left ventricle) - Any increase in flow or decrease in diastole (tachycardia) increases gradient by that squared, and precipitates elevated LAP and pulmonary hypertension. If flow is doubled, then gradient is quadrupled C. Increases myocardial oxygen consumption – true, but may occur in the presence of a heart without IHD Severe MS, if untreated, results in progressive elevations in left atrial pressure, PVR, left atrial size, elevation of the left main stem bronchus, AF, left atrial thrombus formation, and obliterative (and thus irreversible) pulmonary vascular changes and resultant right heart failure. The essential characteristics of a normal MV are: 1. Area greater than 4.0 cm3 2. Diastolic mitral valve flow of 150-200 ml/sec/diastole 3. Diastolic transvalvular pressure gradient of less than 2 mmHg 4. LVEDP of approximately 5 mmHg For any given valve area, the higher the flow, the larger the gradient, but the relationship is not linear, such that a normal valve will not have a significant gradient even if the flow doubles, whereas a valve of 1 cm3 will have a gradient of 18-28 mmHg at normal flow. At any given valve area, the gradient also increases as flow increases. Thus patients with moderate MS are subject to acute elevations in left atrial and pulmonary vascular pressures and thus symptoms when flow increases precipitously (e.g. pregnancy, hypervolemia, hyperthyroidism) and/or diastolic time decreases (e.g.new AF with rapid ventricular response, which differentially shortens diastolic time. The Gorlin formula is used to calculate mitral valve area and requires that the flow and gradient be measured simultaneously. MVA = Mitral flow (ml/sec/diastole) 38√LADM - LVDM Rearranging the formula reveals that flow is proportional to the square of the gradient. Thus if flow is doubled, the trans-valvular gradient will be quadrupled. (or… if the flow is to be doubled the transvalvular gradient needs to increase by a factor of 4) MS is considered mild when the MVA is between 1 and 2 cm2, and critical if less than 1 cm2 ----------- |
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MC53
Prominent U waves in the ECG may be seen in: A. Hypokalaemia B. Wolff-Parkinson-White syndrome C. Mitral stenosis D. Sinus tachycardia D. Hypocalcaemia |
A. Hypokalaemia
and Hypercalcaemia ----------- |
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MC55
The J-point of the ECG waveform is altered by all of the following EXCEPT A. hypothermia B. tachycardia C. myocardial ischaemia D. calcium channel blockers E. digoxin |
D. calcium channel blockers
ECG by example Calcium channel blockers may cause: Sinus bradycardia Junctional bradycardia Wenkebach phenomenon. J point: Point at which the QRS Complex meets the ST Wave ~~ J point ↓ • Hypothermia • Tachycardia • Ischaemia • ↓ CO2 • ↓ K+ • Digoxin • Cardiac surgery ----------- A. hypothermia – Osborn waves, also known as J waves – uneven elevation of J point and ST segment. B. tachycardia – J point looks elevated C. myocardial ischaemia – ST depression lowers J point, ST elevation raises it D. calcium channel blockers – may occur in toxicity though. Most commonly causes bradycardia, junctional rhythm and Mobitz type 1, and other forms of heart block in toxicity. E. digoxin – reverse tick (sloping ST depression) – lowering of J point http://www.hypertension-consult.com/Secure/textbookarticles/Textbook/58_ECG2.htm Hypothermia. When core body temperature approaches 32°C, hypothermia produces alterations in the ECG that might be mistaken for AMI. Most often, hypothermia-related electrocardiographic changes are observed at the junction between the terminal portion of the QRS complex and the initial ST segment (i.e., the J point). The J point and the adjacent ST segment appears to have lifted off the iso-electric baseline. Unlike the J point elevation seen in BER (benign early repolarisation), in which the J point and ST segment are uniformly lifted upward, the J point and adjoining ST segment in hypothermia are unevenly elevated off the baseline. The resulting configuration produces the J wave, also know as the Osborn wave, or the Osborn J wave. (See Figure 35 for an example of an ECG depicting the J wave in a hypothermic patient.) (Table 5.) In the typical situation, the J wave and related STE are most prominent in the mid-precordial and lateral precordial leads; it is seen to a lesser extent in the limb leads. In general, the amplitude of the J wave is inversely proportional to the degree of hypothermia; the J wave will increase in amplitude as the core temperature continues to drop and, conversely, will lessen as successful rewarming progresses. Other electrocardiographic features associated with hypothermia include: bradycardia; tremor artifact; prolongation of the PR and QT intervals; T wave inversions in leads with prominent J waves; and arrhythmias such as atrial fibrillation and ventricular fibrillation.5 http://www.emedicine.com/ped/topic2716.htm - Calcium channel blocker toxicity Electrocardiography o Perform an ECG in all patients presenting to the ED who possibly have ingested any cardiac medication. o Perform an ECG in every patient presenting with a suicide gesture to evaluate for the signs of tricyclic antidepressant (TCA) overdose. TCA toxicity can progress rapidly to malignant arrhythmia if untreated. o ECG changes are neither sensitive nor specific for CCB toxicity. o ECG may reveal bradycardia; tachycardia; first-, second-, or third-degree AV block; any type of bundle-branch block; and nonspecific ST-T wave changes. ECG by example 11 Digoxin effect: ST segments have characteristic down sloping depression (reverse tick) Non specific intraventricular conduction delay. |
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MC58
HOCM. Most decompensation with: (or: Moderate haemodynamic instability with:) A. Moderate decrease in volume B. Increased systemic vascular resistance C. Moderate tachycardia D. Decreased contractility E. Vasoconstriction (Type A) (Related Q AC41, MC70, MC78) |
A. Moderate decrease in volume
B. Increased systemic vascular resistance – same as option E – wrong – DECREASING afterload will worsen obstruction C. Moderate tachycardia – although severe tachycardia is bad, moderate tachycardia would be physiological D. Decreased contractility – definitely wrong – decompensation with INCREASED contractility E. Vasoconstriction – definitely wrong - worse with vasodilation Maintain • Sinus rhythm • Slow HR • High afterload • Full preload Avoid increased contractility ----------- |
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MC59 [Aug12]
The treatment LEAST likely to be useful for torsades de pointes is A. defibrillation B. procainamide C. magnesium D. electrical pacing E. isoprenaline |
B. procainamide
~~ Avoid Class I anti-arrhythmics, mexilitine & sotalol (in renal failure) Magnesium – first line treatment according to emedicine Isoprenaline – second line treatment according to emedicine Lignocaine – has been used to treat resistant TDP Phenytoin – useful, as it shortens the QTc – according to Harrisons β blockade is the mainstay for congenital prolonged QT (Lown Ganong Levine) – remember that fat Med Reg in Dunedin on his first on call night in Nelson ----------- M6,1404 Torsades de pointes, which may mimic VF or VT, is a life threatening arrhythmia that occurs in the presence of disturbed repolarisation (hence its association with prolonged QT interval). Discontinuation of drugs that predispose to QT interval prolongation and correction of electrolyte abnormalities are essential in the treatment of torsades de pointes. Acute therapy may include defibrillation, 1 to 2g of intravenous magnesium sulfate, amiodarone (n.b not considered a good therapy in most texts ), isoprenaline and overdrive pacing. By mechanisms that are poorly understood, mexiletine may exacerbate existing arrhythmias and may evoke torsades de pointes. AMIODARONE - prolongation of the QT interval is commonly observed during chronic treatment but induction of torsades de pointes is seen only rarely. The most important unwanted effect of sotalol may be its arrhythmogenic activity, which includes provoking torsades de pointes. The likelihood of this effect is increased by hypokalaemia, and is greater in women than in men. Since sotalol is eliminated mainly by excretion, unchanged in the urine, the danger of torsades de pointes is also increased where there is renal dysfunction. http://www.lhsc.on.ca/critcare/icu/cctc/procprot/pharmacy/mono2/procainamide.html Adverse Effects of procainamide Cardiac: o arrhythmias: ventricular tachycardia or fibrillation, Torsades de Pointes (associated with high levels of procainamide and/or NAPA (N-acetyl procainamide); secondary to prolonged QT interval) o heart block o prolongation of PR, QRS, QT intervals (up to 50%) o bradycardia, asystole o decreased BP, decreased |
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MC59b ANZCA version [2003-Apr][2003-Aug][2005-Sep] Q69, [Mar06][Apr08][Oct08][Mar10] [Aug10][Sep11]
In the management of torsades de pointes (polymorphic ventricular tachycardia), all the following drugs may be useful EXCEPT A. amiodarone B. isoprenaline C. lignocaine D. magnesium E. phenytoin |
A. Amiodarone
see wiki debate. and my note. ? E. phenytoin ? "with regards to 59b version I'm torn between amiodarone and phenytoin. The ARC guidelines (Guideline 11.9) state that amiodarone should be avoided but they also state that torsades leading to cardiac arrest is managed according to the cardiac arrest algorithm ... which includes using amiodarone? ILCOR 2010 Guidelines pg e105 state "Among patients with impaired ventricular function due to structural heart disease, in the absence of QT prolongation or drug provocation, treatment of haemodynamically unstable VT with IV amiodarone reduced the frequency of recurrent arrhythmias. This evidence rests on extrapolation from three prospective RCTs (LOE5) performed in the in-hospital setting but in which VT morphology was not addressed specifically." Hopefully if this question is asked again the specifics of the type of polymorphic VT is outlined as the treatment options seem to vary depending on whether it is congenital, aquired, ischaemic or just unknown. -- drfpc dec 2012" suggest reading CoSTR 2010 e105 ----------- |
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MC65 ANZCA version [2002-Mar] Q53, [2002-Aug] Q63, [2004-Apr] Q59, [2004-Aug] Q84, [2005-Sep] Q58, [Mar06] Q38, [Jul07]
Characteristic cardio-pulmonary effects of pulmonary thromboembolism include A. hypoxaemia due to excess perfusion of lung units with a low V/Q ratio B. hypercarbia due to an increase in physiological dead-space C. reverse splitting of the second heart sound D. an increase in compliance of the left ventricle E. an increase in coronary blood flow to the right ventricle during systole |
A. hypoxaemia due to excess perfusion of lung units with a low V/Q ratio
----------- The main causes of hypoxaemia in pulmonary embolism seem to be as follows: (1) Ventilation-perfusion mismatch. Unembolised areas of the lung are relatively overperfused (creating low VQ ratios), so that the ventilation in these areas may be insufficient to oxygenate fully the extra blood flow. (2) Shunting occurs through areas of collapse and infarction (secondary to emboli) that are not ventilated but retain some blood flow. This may become more important a few days after the initial episode. In patients with a patent foramen ovale, raised right atrial pressure may open the foramen and cause right-to-left shunting at the atrial level. This should be considered if the degree of hypoxaemia is more profound than would be expected from other clinical features, if it cannot be corrected by oxygen administration and if it is accompanied by hypercapnia. (3) Low mixed venous oxygen saturation caused by the reduced cardiac output causes hypoxaemia because there is insufficient time for the extremely desaturated blood to become fully saturated as it passes through the alveolar capillaries in the overperfused areas of the lung. Although pulmonary embolism impairs the elimination of CO2, hypercapnia is rare because compensatory hyperventilation eliminates CO2 in all but the most extensive embolism. In cases with a sufficient degree of vascular obstruction to produce hypercapnia, the haemodynamic sequelae of acute right ventricular failure usually prove fatal. |
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MC70
Which of the following drugs is/are contraindicated in patients with HOCM? A. Amrinone B. Esmolol C. Sotalol D. Metaraminol E. ? Beta-blockers F. Thiopentone (Related Q AC41 & MC58) |
A. Amrinone
Maintain • Sinus rhythm • Slow HR • High afterload • Full preload Avoid increased contractility ----------- |
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MC70c ANZCA version [2001-Apr] Q92
During anaesthesia, a patient with hypertrophic obstructive cardiomyopathy (HOCM) develops hypotension and the pulse oximetry reading falls to 91%. Appropriate management includes 1. administration of intravenous fluid 2. addition of positive end-expiratory pressure (PEEP) 3. administration of metaraminol 4. administration of dopamine |
1 & 3
Dopamine is to be avoided as this is an inotropic agent (See above) If you need an antiarrythmic digoxin is a bad idea (inotrope), amiodarone, disopyramide, sotalol recommended. Anything that causes a rapid fall in venous tone (eg GTN, SNP) will increase outflow obstruction: PEEP is to be avoided. This increases intrathoracic pressure, reducing RV output and hence LV preload. Hypotension should be treated with positioning (Trendelenburg), volume replacement [increases LV filling] and vasoconstrictors that are not inotropes as well eg phenylephrine. (Kaplan. Cardiac Anesthesia 4th ed. p914, Roizen p 69) ----------- |
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MC74
The best initial management of SVT if not haemodynamically compromised is: A. Carotid sinus massage B. Valsalva manoeuvre C. Cardiovert with patient awake D. Induce GA and cardiovert E. IV Verapamil |
B. Valsalva manoeuvre
a study published in the Lancet 1988 1:1181-5 which demonstrated that Valsalva is most effective vagal maneouvre. ----------- |
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MC76 [Oct08]
Which new change on ECG is most likely to indicate acute ischaemia? A. 2mm horizontal ST depression in 60yr old male undergoing TURP with spinal B. 2mm ST depression in previously fit 20yr old female GA caesarean C. 0.7mm ST depression in a 60 yr old male undergoing TURP with spinal D. 2mm downsloping ST depression in 30yr old male craniotomy for SAH E. T-wave inversion in 60yr old male TURP under spinal (see also MC87)s |
A. 2mm horizontal ST depression in 60yr old male undergoing TURP with spinal
~~ Miller 6th ed. p1405 TABLE 34-7 -- Electrocardiographic criteria for ischemia in anesthetized patients --------------------------------------------------------------------- • Upsloping ST segment: 2-mm depression, 80 msec after J point • Horizontal ST segment: 1-mm depression, 60–80 msec after J point • Downsloping ST segment: >1 mm from top of curve to PQ junction • ST elevation • T-wave inversion ----------- Electrocardiographic changes in patients with acute stroke: a systematic review. Repolarization and ischemic-like electrocardiographic (ECG) changes observed during acute phase of stroke may cause diagnostic and management dilemmas for the clinician. In this systematic review, we have compiled all information available in the literature on the prevalence of these ECG changes and QT prolongation during the acute phase of stroke and their coexistence with other abnormal cardiac findings. Abnormalities, such as ischemic-like ECG changes and/or QT prolongation, were found in 76% (95% CI 73-90) of patients with subarachnoid hemorrhage, irrespective of whether they had preexisting heart disease or not. Such ECG changes were present in more than 90% of unselected patients with ischemic stroke and intracerebral hemorrhage, but the prevalence was much lower after exclusion of patients with preexisting heart disease. Compared with other abnormal cardiac findings (cardiac wall motion abnormality detected by echocardiography, elevated levels of biochemical markers of myocardial injury, autopsy findings, thallium scintigraphy), these ECG changes were characterized by a high sensitivity but a very low specificity. Thus, in patients with subarachnoid hemorrhage, repolarization and ischemic-like ECG changes are mainly direct consequences of the cerebral condition and their absence essentially rules out cardiac abnormalities. In patients with ischemic stroke and intracerebral hemorrhage, these ECG abnormalities (and QT prolongation) most often represent preexisting coronary artery disease. The specificity of ECG changes to diagnose acute myocardial infarction is low in the acute phase of stroke. Copyright 2002 S. Karger AG, Basel Cerebrovasc Dis. 2002;14(2):67-76 |
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MC79
When anaesthetising a patient with an acute pericardial tamponade, A. the patient may be safely induced with a dose of 3-5 mg.kg-1 of thiopentone B. it is important to limit intravenous fluid infusion, to prevent further compression of the heart C. it is important to reduce afterload D. a slow heart rate allows time for optimal filling of the ventricle E. awareness is a potential problem after release of the tamponade |
E. awareness is a potential problem after release of the tamponade
~~ Avoid • ↓ SVR - you drop the diastolic, poor coronary perfusion • ↓ HR - NO, CO is limited by SV, so keep HR high • ↓ venous return - need filling pressure • ↓ contractility ----------- A. – ketamine or etomidate better – STP is myocardial depressant and this is a full dose. B. – need to fill C. - SD says to use ketamine because it increases SVR. Miller says to minimise SVR drops D. – need tachycardia to increase output. (tamponade keeps SV low) E. - awareness is a potential problem after release of the tamponade – because of light anesthesia GA and IPPV in the presence of haemodymanically significant tamponade can result in life-threatening hypotension. Reasons include anaesthetic induced vasodilation, myocardial depression, and decreased venous return. Pericardiocentesis under LA is preferred. When not possible, the goal of anaesthesia must be to maintain cardiac output. Ketamine is useful for induction and maintenance of anesthesia as it increases myocardial contractility, systemic vascular resistance, and the heart rate. Induction with benzos, followed by maintenance with nitrous and fentanyl and panc has been used successfully. Use CVP and IAL monitoring. Isoprenaline, dopamine or dobutamine may be useful for maintaining CO until the tamponade can be relieved by surgical drainage. Miller 2nd ed p1773 The plan should include monitoring of the important hemodynamic variables, and it should omit drugs and minimize manipulations that decrease VR, reduce HR, produce hypotension, result in hypoxemia, or impair ventricular contractility. Particular attention should be made to the mode of ventilation; positive pressure ventilation further embarrasses venous return and cardiac output. Spontaneous ventilation should be maintained until the tamponade is relieved. Positive measures such as expansion of the circulating blood volume, infusion of an inotrope, and maintenance of a high oxygen content of arterial blood are often beneficial |
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MC80
The transplanted heart A. May be two P waves on ECG B. Not responsive to adrenaline or isoprenaline C. The heart does not respond to preload by the normal Starling mechanism D. Arrhythmias unlikely E. Resting bradycardia (Also remembered as: "The cardiac transplant recipient for non-cardiac surgery. . ") |
A. May be two P waves on ECG
The SA node is located between the junction of the SVC and right atrium. This portion of tissue is often left behind when the original heart is removed. Hence on 12 lead ECG it is possible to see two P waves. ----------- |
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MC81
A low ejection fraction is most likely to be seen in a patient with A. poor left ventricular (LV) systolic function B. poor LV systolic function and severe mitral regurgitation C. poor LV diastolic function D. septic shock E. a post myocardial infarct ventricular septal defect |
A. poor left ventricular (LV) systolic function
% EF = (EDV - ESV) / EDV Yes. Definition EF = (EDV-ESV)/EDV MR decreases ESV as blood heads into the low pressure LA therefore MR gives you a better EF. Better on paper that is. ----------- |
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MC84a [Mar11]
In patients with Eisenmenger's Syndrome, A. compensation for poor oxygenation at rest is achieved by an increase in cardiac output B. the high pulmonary vascular resistance is usually able to be treated with a specific vasodilator C. an Fi02 of 1.0 will produce a substantial improvement in Sa02 D. the usual clinical course includes right ventricular failure during the 3rd or 4th decade, and subsequent death E. venesection should be used to treat a haemoglobin greater than 180 g.l-' to prevent the problems of hyperviscosity |
D. the usual clinical course includes right ventricular failure during the 3rd or 4th decade, and subsequent death
- they USUALLY die in 30's B - may help but not 'usually' E - venesection may help but unsure of ideal HCT A rare syndrome of pulmonary hypertension associated with a reversed or bidirectional cardiac shunt, occurring through a large communication between the left and right sides of the heart. The defect may be interventricular, interatrial, or aortopulmonary. The development of Eisenmenger’s syndrome, from the initial left to right shunt, is usually a gradual process. Contributory factors to the pulmonary hypertension are hypoxia, high pulmonary blood flow, and high left atrial pressure. Irreversible structural changes take place in the small vessels, causing pulmonary vascular obstruction and a reduction in the size of the capillary bed. The pulmonary artery pressure is the same as, or sometimes exceeds, the systemic arterial pressure. COmpensate for hypoxia by erythrocytsis, usually die 2-4th decade Principles of Management for Anaesthesia ------------------------------------ • Maintain adequate circulating blood volume • HIGH SVR • LOW PVR - myocardial depressants and peripheral vasodilators should be used with caution - bradycardia must be prevented - avoid hypotension with if regional anaesthesia is used • IPPV with low inflation pressures (+ early extubation). • Air must be completely eliminated from all intravenous lines and the epidural space should be located with loss of resistance to saline, not to air. • Appropriate antibiotics prophylaxis to prevent bacterial endocarditis. ----------- Yao241 The main goal of induction in a cyanotic patient is to establish necessary levels of anesthesia without increasing the right to left shunt. The stress of the induction can lead to a hypercyanotic spell. Objectives are to: o Maintain SVR. Avoid drugs that decrease SVR and treat decreases with vasoconstrictors o Decrease PVR to maintain or improve PBF. Hypercarbia, hypoxia, light anesthesia, atelectasis, polycythemia, acidosis and elevated airway pressures INCREASE PVR. Hypocarbia, anemia, alkalosis, high oxygen concentrations, and deep anesthesia DECREASE PVR. PVR can also be decreased using drugs such as GTN, SNP, phentolamine, tolazoline, PGE2, or inhaled NO o Favour mild myocardial depression and euvolemia because they can help prevent or limit a hypercyanotic spell. Most volatile anesthetics provide some myocardial depression with halothane having the most profound effect. o Slow heart rate to reduce the likelihood of infundibular spasm. Induction can be accomplished with ketamine 2mg/kg or fentanyl 25/kg. An iv induction is faster in patients with a right to left shunt because peak receptor site concentrations are attained faster (no need to go through the lungs). Inhalational induction with sevo or halothane is always a possibility, bearing in mind that a significant right to left shunt may delay induction (less flow through the lungs, and unable to use nitrous due to increased PVR – no second gas effect). THE EFFECTS OF SOME DRUGS: Barbiturates vasodilate, lowering SVR and PVR Ketamine decreases PVR in adults, but not kids. Its’ sympathomimetic effect helps in maintaining SVR, and it is considered one of the safest induction techniques for a cyanotic patient. Opioids provide good hemodynamic stability without altering PVR. Fentanyl and sufentanil are used for maintenance of anaeshtesia because they blunt the sympathetic stress response Halothane and sevo are both considered safe for inhalation induction. They both decrease SVR but have a small effect on PVR. Sevoflurane is less of a myocardial depressnat than halothane. Des and iso decrease SVR in a dose dependent manner and are mild myocardial depressants. Des at higher concentrations (above 6%) is associated with increased sympathetic stimulation, which can be detriminetal in cyanosis. Nitrous won’t increase PVR in children, but 100% oxygen is preferred to avoid hypoxia. |
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MC84c ANZCA version [2005-Apr] Q49, [2005-Sep] Q67 [Apr08][Oct08]
In providing anaesthesia for a patient with Eisenmenger's syndrome, it is NOT true that A. an important goal is to maintain an optimal shunt, by preventing changes to pulmonary vascular resistance (PVR) or systemic vascular resistance (SVR) B. the patient's high haemoglobin should be maintained and blood loss monitored closely C. a gaseous induction with sevoflurane presents an effective method for anaesthesia and avoids cardiovascular compromise D. if general anaesthesia is required, ketamine is an - appropriate choice of drug E. careful attention to intravenous infusions and drug administration is needed to prevent paradoxical air embolism |
C. a gaseous induction with sevoflurane presents an effective method for anaesthesia and avoids cardiovascular compromise
?or B. see wiki debate. Re: C - wording of "avoids" is too absolute. ----------- |
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MC85
In a patient undergoing a femoro-popliteal bypass, the most predictive independent risk factor for the development of post-operative myocardial infarction would be A. a previous history of coronary artery bypass grafts B. diabetes mellitus C. an episode of intraoperative myocardial ischaemia D. hypercholesterolaemia E. an episode of post-operative myocardial ischaemia lasting over 60 minutes |
E. an episode of post-operative myocardial ischaemia lasting over 60 minutes
• Peri-op myocardial ischeamia peaks in the early post-op period and is significantly associated with MI and cardiac complications. Intraop ischaemia is less common and infrequently associated with post-op MI. • Peri-op MI is almost exclusively preceded by ST depression type ischaemia (STEMI is uncommon) • Peri-op MI is mostly silent (only 50% have any Sx) and occur in first 24-48 hours post-op- pick up with cont. ECG monitoring and ST trend analysis and troponin. Landesberg G: The pathophysiology of peri-op MI: the facts and perspectives. J Cardiothoracic and Vasc Anaes 2003: 17(1): 90-100 ----------- |
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MC87
ECG criteria for diagnosis of ischaemia in anaesthetised patients include the presence of 1. an upsloping ST segment with 2 mm depression, 80 msec after the J point 2. a horizontal ST segment with > 1 mm depression, 60 to 80 msec after the J point 3. a downsloping ST segment with > 1 mm depression, 60 to 80 msec after the J point 4. ST segment elevation of > 1mm |
All of the above
Miller 6th ed. p1405 TABLE 34-7 -- Electrocardiographic criteria for ischemia in anesthetized patients ------------------------ • Upsloping ST segment: 2-mm depression, 80 msec after J point • Horizontal ST segment: 1-mm depression, 60–80 msec after J point • Downsloping ST segment: >1 mm from top of curve to PQ junction • ST elevation • T-wave inversion ----------- |
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MC88
Use of cardioversion for atrial fibrillation: A. Size of left atrium is best predictor B. Increased defibrillation threshold if on Class 1 antiarrhythmics C. CK rise seen after defibrillation D. Need high serum levels of digoxin |
C. CK rise seen after defibrillation
~~ • Following electrical cardioversion of atrial fibrillation or atrial flutter, cardiac troponin T remains unchanged despite a large rise in total CK, indicating that the CK is derived from skeletal muscle and that myocardial injury does not occur. (Heart 1998;80:226-228) LA size IS NOT a predictor of successful cardioversion Success rate IMPROVED on class 1 drugs C. CK rise seen after defibrillation – best answer, although below it says cardiac enzymes are usually normal after DCC DCV Contraindicated if dig toxic B.Increased defib threshold if on class 1 antiarrhythmics- False (same article) class1a drugs may increase the success rate C.CK rise after defib (same article) -False -cardiac enzymes are usually normal after DC cardioversion D.Need high serum levels of digoxin- False (as above) -cardioversion should not be performed if dig levels are above the therapeutic range. ----------- Direct current cardioversion should not be performed if the patient has digoxin levels above the therapeutic range. The energy requirements are usually in the 25 100 J range but occasionally higher energy shocks (200 J) are required, particularly if the duration of the atrial fibrillation is less than 24 h [43]. Left atrial size is not a predictor of successful cardioversion. However, the success rate is greater with arrhythmias of short duration [43 45]. Prior treatment with class Ia anti-arrhythmic drugs such as quinidine or disopyramide may increase the success rate [46]. ST segment changes following cardioversion occur in up to 19% of patients, particularly in those patients who have undergone cardiac surgery [47]. However, there is no evidence of myocardial damage and cardiac enzymes are usually normal after DC cardioversion. The peri-operative management of atrial fibrillation (Anaesthesia 1998; 53: 665) |
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MC89
With regard to atrial fibrillation (AF), which of the following is true? A. Most common arrhythmia during surgery B. Causes more hypotension in a patient with aortic stenosis than mitral regurgitation C. Associated with a steep x descent on CVP trace / or: loss of x descent D. Can be treated with carotid sinus massage E. Should be treated with dantrolene (see also MC101) |
B. Causes more hypotension in a patient with aortic stenosis than mitral regurgitation
(pjs I disagree - No. 2 in management of MS is "maintain sinus rhythm" - it's VERY bad in MS, as there's more blood to get into the ventricle in diastole due to the reverse flow.) * Severe AS - low ejection fraction as it can't get out - the ventricle is still partially filled at end systole * x descent is due to atrial diastole - so if this is an option, definately true. Tachycardia and loss of atrial kick - well, they didn't say it's rapid... ----------- |
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MC93b
Aortic valve stenosis is more likely to be severe if A. a loud second heart sound is present B. an ejection click is heard C. a third heart sound is present D. the murmur is long in duration and peaks late in systole E. the systolic murmur is transmitted to the carotid arteries |
D. the murmur is long in duration and peaks late in systole
Signs of Severe AS (valve area < 1cm2 or gradient > 50-70 mmHg) ---------------- • plateau pulse • thrill in aortic area • length of the murmur and lateness of the peak of the systolic murmur • S4 • Paradoxical splitting of S2 (greatly delayed Aortic valve closure) • Absent A2 • LVF (very late) (Talley & O'Conner) ----------- |
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MC93c ANZCA version [2005-Apr] Q110
All of the following clinical findings suggest the diagnosis of aortic stenosis EXCEPT A. an early systolic murmur B. brachioradial pulse delay C. decreased intensity or absence of S2 (second heart sound) D. decrease in murmur intensity with a Valsalva manoeuvre E. effort syncope |
A. an early systolic murmur - ?all other options are definitely true (so not the answer)
B. brachioradial pulse delay - true "During the assessment of patients with severe or symptomatic aortic stenosis, a clinically detectable delay between the brachial and radial pulses was observed. This delay was not present in normal subjects. The timed delay of 53.5 (SE 2.6) ms in severe aortic stenosis was significantly longer than that in normal volunteers 22.6 [1.3] ms) or in patients with low cardiac output. This increased delay was clinically detectable before the occurrence of left ventricular failure and often before the onset of symptoms." (Brachioradial delay and severity of aortic stenosis. Caro CG, Parker KH. Lancet. 1990 Jun 23;335(8704):1535) C. decreased intensity or absence of S2 (second heart sound) - true: "S2 is soft and single since A2, which is due to aortic valve closure, is delayed and tends to occur simultaneously with P2, which is due to pulmonic valve closure. The S2 may become paradoxically split when the stenosis is severe and associated with left ventricular dysfunction (movie 1). With increasingly severe, fixed AS, the A2 closing sound may disappear. The presence of a normal split S2 is the most reliable finding to exclude severe AS in adults" (Uptodate, Pathophysiology and clinical features of valvular aortic stenosis in adults) D. decrease in murmur intensity with a Valsalva manoeuvre - true "Both the intensity of the murmur and the carotid pulse volume decline with Valsalva in AS" (Uptodate, Auscultation of cardiac murmurs) E. effort syncope - true ----------- |
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MC95
The most important pre-operative investigation in a non-anticoagulated patient with chronic atrial fibrillation undergoing direct cardioversion is A. chest x-ray B. electrocardiograph (ECG) C. serum digoxin level D. serum potassium level E. transoesophageal echocardiography |
E. transoesophageal echocardiography
~~ ----------- AF Duration < 48hours: Immediate cardioversion ------------------------------------------ There is a low risk of systemic embolization if the duration of the arrhythmia is 48 hours or less and there are no associated cardiac abnormalities (particularly mitral valve disease or significant LV enlargement due to a cardiomyopathy). In such patients, electrical or pharmacologic cardioversion can be attempted after systemic heparinization. AF Duration > 48 hours: two options ------------------------------- Option One: Conventional approach - It is preferable to anticoagulate with warfarin for approximately three to four weeks before attempted cardioversion to allow any left atrial thrombi to resolve if: • The duration of AF is more than 48 hours or of unknown duration • There is associated mitral valve disease or significant cardiomyopathy or HF • The patient has a prior history of a thromboembolic event During this time, rate control should be maintained with an oral AV nodal blocker as described above. Option Two: TEE-guided Approach - Among patients with AF of recent onset (but more than 48 hours) who are not being anticoagulated, an alternative approach to three to four weeks of warfarin therapy before cardioversion is TEE-based screening with cardioversion performed if no thrombi are seen. This regimen may be of particular use in the patient who requires hospitalization or has an increased risk of hemorrhagic complications during prolonged warfarin therapy (eg peri-operatively). |
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MC100
A 24 year old female with mitral valve prolapse develops atrial flutter during a diagnostic laparoscopy. The drug most likely to revert this arrhythmia is A. digoxin B. amiodarone C. verapamil D. esmolol E. Adenosine |
B. amiodarone
~~ A. digoxin – used in rate control but not for cardioversion B. amiodarone C. verapamil – used in rate control but not cardioversion D. esmolol – sotalol used in rate control but not cardioversion E. Adenosine – used to diagnose AFlutter ----------- General goals for the treatment of symptomatic atrial flutter are similar to those for atrial fibrillation and include: (1) control of the ventricular rate (2) termination of sustained episodes (3) prevention and decreased frequency or duration of recurrent episodes (4) prevention of thromboembolic complications (5) minimization of adverse effects from therapy. Electrical cardioversion -------------------- The success rate of electrical cardioversion is higher than 95%. • Factors to consider include synchronization of shocks to R waves, adequate sedation, and electrode position (apex anterior, apex posterior, anteroposterior). • Atrial flutter generally requires less energy for conversion than atrial fibrillation, and as few as 50 joules may be necessary. Recent data show that an initial energy of 100 joules is more effective and is less likely to induce atrial fibrillation than 50 joules. • If cardioversion is not successful with one electrode configuration, switching may improve success. A second set of electrodes can be used with tandem or simultaneous shocks. • Newer devices with different outputs and biphasic external waveform may be more effective in restoring sinus rhythm. • A few points to remember about the cardioversion technique include a wide electrode separation in the anteroapex position, the application of pressure on paddles or electrodes to reduce thoracic impedance, and the placement of electrode patches under or lateral to the breasts in women. Pharmacological cardioversion -------------------------- • Procainamide is effective for converting atrial flutter to sinus rhythm in 0-13% of patients. • Flecainide is effective in approximately 10% of patients. • Dofetilide is effective in 70-80% of patients. • Ibutilide is effective, converting recent-onset atrial flutter to sinus rhythm in 63% of patients with a single infusion. • Large single oral doses of type IC antiarrhythmic agents, such as propafenone (450-600 mg) or flecainide (200-300 mg), have also been shown to be effective in converting recent-onset atrial fibrillation to sinus rhythm. Their use in atrial flutter can be assumed to have at least equal success. • Oral amiodarone during the loading period (>1 mo) converted 18% of atrial fibrillations or flutters to normal sinus rhythms. Intravenous amiodarone is also effective in converting atrial flutter to sinus rhythm and in slowing the ventricular rate in patients with a rapid ventricular response. |
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MC102
A permanent pacemaker is indicated in the asymptomatic patient with 1. complete heart block following acute inferior myocardial infarction 2. sick sinus syndrome 3. Wenckebach atrioventricular block 4. Mobitz Type II atrioventricular block |
4. Mobitz Type II atrioventricular block
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MC104 ANZCA Version [Apr 08]
It is MOST important to re-program a patient's implanted cardiac pacemaker prior to: A. electroconvulsive therapy (ECT) B. laser therapy to a laryngeal papilloma C. lithotripsy of a renal calculus D. magnetic resonance imaging of the thorax E. percutaneous transhepatic cholangiography |
C. lithotripsy of a renal calculus
also A. ECT and MRI if compatible - read Yao and Artusio Ch. 9 ----------- Situations Probably Requiring Pacemaker Reprogramming Any rate-responsive device—see text (problems are well known[23,45] and have been misinterpreted with the potential for patient injury[46-49]; the Food and Drug Administration has issued an alert regarding devices with minute ventilation sensors[50]—see Box 43-4) Special pacing indication (hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy, pediatric patients) Pacemaker-dependent patients Major procedure in the chest or abdomen Rate enhancements present that should be disabled Special procedures (see text) Lithotripsy Transurethral resection Hysteroscopy Electroconvulsive therapy Succinylcholine use Magnetic resonance imaging (generally contraindicated by device manufacturers)[51] In some situations and for certain patients, a pacemaker should be reprogrammed either to avoid potential patient injury or to prevent a pacemaker rhythm that could be confused with pacemaker malfunction. |
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MC106
A patient with pulmonary hypertension secondary to lung disease presents for laparotomy. The anaesthetic technique LEAST likely to exacerbate the pulmonary hypertension is endotracheal intubation and A. controlled ventilation with isoflurane, N2O and O2 B. spontaneous breathing with isoflurane and O2 / air C. controlled ventilation with total intravenous anaesthesia and O2 / air D. controlled ventilation with ketamine and O2 / air E. controlled ventilation with high dose opioids, N2O and O2 |
C. controlled ventilation with total intravenous anaesthesia and O2 / air
Factors the increase PVR: • Low FiO2 • Acidosis • Hypercarbia • Sympothomimetics • High positive end-expiratory pressure ----------- |
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MC107
A permanent dual-chamber transvenous pacemaker set to a DDDR mode will A. NOT be affected by diathermy B. increase the ventricular pacing rate if the minute volume is increased C. usually require reprogramming to VVO mode for surgery D. revert to DDD mode if a magnet is placed over the generator site E. result in a tachyarrhyrthmia if the patient develops atrial flutter |
B. increase the ventricular pacing rate if the minute volume is increased
also E. result in a tachyarrhyrthmia if the patient develops atrial flutter see wiki discussion •D ual Chamber Pacing •D ual Chamber Sensing •D ual (Trigger & Inhibit) •R ate Modulation ----------- |
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MC109 [Apr08][Oct08]
In patients with mitral regurgitation A. left ventricular damage does NOT occur before the onset of symptoms B. mitral valve replacement has a lower operative mortality and incidence of late adverse outcomes compared to mitral valve repair C. an ejection fraction of less than 60% may be an indication for surgery, even in the absence of symptoms D. long term vasodilators have been shown to delay the need for surgery E. the presence of a third heart sound always indicates heart failure |
C. an ejection fraction of less than 60% may be an indication for surgery, even in the absence of symptoms
"asymptomatic patients at less than 60% may require surgery." (Core Topics in Anaesthesia) "Surgical treatment of severe MR should be considered even in asymptomatic patients or those with mild symptoms when LV dysfunction is progressive, with LV EF declining below 60% and/or end-systolic cavity dimension on echocardiography rising above 45 mm." (Harrisons Online, Chapter 219) ----------- In patients with mitral regurgitation A. left ventricular damage does NOT occur before the onset of symptoms - false: "Unlike stenotic cardiac valve lesions, regurgitant cardiac valve lesions often progress insidiously, causing left ventricular damage and remodeling before symptoms have developed." (Stoelting) B. mitral valve replacement has a lower operative mortality and incidence of late adverse outcomes compared to mitral valve repair - false: "Mitral valve repair is preferred to mitral valve replacement because it restores valve competence, maintains the functional aspects of the mitral valve apparatus, and avoids insertion of a prosthesis." C. an ejection fraction of less than 60% may be an indication for surgery, even in the absence of symptoms - true: "Survival may be prolonged if surgery is performed before the ejection fraction is less than 60% or before the left ventricle is unable to contract to an end-systolic dimension of 45 mm (normal < 40 mm). Symptomatic patients should undergo mitral valve surgery even if they have a normal ejection fraction." (Stoelting Ch2) D. long term vasodilators have been shown to delay the need for surgery - false: "Although vasodilators are useful in the medical management of acute mitral regurgitation, there is no apparent benefit to long-term use of these drugs in asymptomatic patients with chronic mitral regurgitation." E. the presence of a third heart sound always indicates heart failure - false: "S3 can be heard and recorded in healthy young adults. However, it is usually abnormal in patients over the age of 40 years, suggesting an enlarged ventricular chamber" (Uptodate) |
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MC110 [Aug10]
Left bundle branch block (LBBB) on the ECG is A. commonly a normal variant B. associated with a delay in atrio-ventricular conduction C. demonstrated by a notched R wave in chest lead V1 D. associated with right axis deviation E. a relative contra-indication to flotation of a pulmonary artery catheter |
E. a relative contra-indication to flotation of a pulmonary artery catheter
- From wiki: A False - due to IHD or LVH (RBBB can be normal variant) B ?False - bundle branch blocks are after the AV node C False - LBBB has notched R in I,III,VL,VF,V5 (Hampton ECG in Practice p272) D False - but RBBB associated with right axis deviation E True - 5% of IHD patients get RBBB on PAC insertion ∴ relative contraindication ----------- |
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MC112
In patients undergoing vascular surgery, myocardial ischaemia is most likely to occur A. in the pre-operative period B. during induction of anaesthesia C. intra-operatively, prior to revascularisation D. in the first 48 hours post-operatively E. 48 to 72 hours post-operatively |
D. in the first 48 hours post-operatively
"A study using continuous 12-lead electrocardiographic monitoring reported 67% of ischaemic events started within 2 hours from the end of surgery and emergence from anaesthesia." Miller, 6th Ed, page 2065 ----------- |
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MC113
When assessing a patient with unstable angina, the clinical feature most predictive of an adverse short-term outcome (death or myocardial infarction within 6 months) is A. increased angina frequency or severity B. angina provoked at a lower threshold of exercise C. new onset angina on effort D. an angina episode lasting more than 10 minutes E. age less than 65 years |
A. increased angina frequency or severity
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MC114 [Mar12]
In Wolff-Parkinson-White (WPW) syndrome, A. the delta wave is caused by a delay in conduction in the accessory pathway B. the PR interval is of normal duration but the QRS complex is widened C. a narrow complex supraventricular tachycardia (SVT) is the most common form of arrhythmia D. central venous cannulation is unlikely to trigger SVT E. cardioversion of arrhythmias is seldom effective |
C. a narrow complex supraventricular tachycardia (SVT) is the most common form of arrhythmia
~~ • WPW is the most common preexcitation syndrome • Accessory connections between the atrium and ventricle bridge the fibrous tissues that separate the two chambers circumvents the usual conduction delay at the AV node and predisposes the patient to develop tachydysrhythmias. • The classic ECG morphology of Wolff-Parkinson-White (WPW) syndrome is described as a shortened PR interval and a widened QRS complex with a delta wave. • The two most arrhythmias are circus movement tachycardia (CMT) - narrow comples tachycardia - and AF • Cardioversion should be the first-line treatment if patient haemodynamically unstable. • Medical management includes beta blockers or sotalol, procainamide • Digoxin, diltiazem, verapamil contraindicated • There are case reports of central venous cannulation triggering SVT http://www.emedicine.com/emerg/topic644.htm ----------- Circus movement Tachycardia = A critically timed premature atrial beat that occurs during the refractory period of the accessory pathway typically initiates CMT. The impulse, therefore, travels solely down the AV node but returns retrograde through the accessory pathway, resulting in CMT (orthodromic conduction). It results in a narrow complex heart rhythm limited by the refractory period of the AV node. The QRS interval is narrow because the impulses travel antegrade (orthodromically) through the AV node and regular because circus movement occurs at a regular rate. http://www.emedicine.com/emerg/topic644.htm |
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MC115
With respect to acute myocardial infarction A. true posterior infarcts manifest on the ECG as a tall R wave in Lead V3 B. aspirin should NOT be given unless myocardial infarction is confirmed C. regional anaesthesia is NOT recommended if thrombolytic therapy has been used within the previous 2 weeks D. Angiotensin Converting Enzyme (ACE) inhibitors may be indicated in the acute period E. Troponin I testing is unsuitable in the perioperative period |
D. Angiotensin Converting Enzyme (ACE) inhibitors may be indicated in the acute period
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MC116 ANZCA version [2003-Apr] Q118
Peri-operative cardiac morbidity and mortality in patients with coronary artery disease undergoing non-cardiac surgery is significantly reduced by A. ceasing smoking one month pre-operatively B. controlling moderate systemic hypertension pre-operatively C. delaying surgery for one month following percutaneous transluminal coronary stent insertion D. delaying surgery for three months following an uncomplicated myocardial infarction E. tight peri-operative control of blood sugar level in diabetic patients |
D. delaying surgery for three months following an uncomplicated myocardial infarction
see wiki. likely question will change in future <3 months 20-30% risk of perioperative MI 3-6 months 10-20% risk >6 months 4-5% risk In a large survey at the Mayo Clinic covering 32,877 patients who had had surgery during 1966-8 there were 422 with previous myocardial infarcts and, of these, 6.6% suffered a further infarct during the first postoperative week. Those operated on within three months of infarction had a 37% reinfarction rate; this fell to 16% after three months and 4.5% after six months. (BMJ, vol 284 20 March 1982) ----------- |
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MC117
The medical therapy for unstable angina which is most effective in reducing progression to myocardial infarction is A. aspirin B. beta-blockers C. calcium channel blockers D. glyceral trinitrate E. thrombolytic therapy |
A. Aspirin
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MC118 [Apr08][Oct08]
An elective surgical patient with hypertrophic obstructive cardiomyopathy becomes hypotensive (systolic pressure 70 mmHg and heart rate 60 beats.min-1) during intravenous induction of anaesthesia. The most appropriate initial therapy would be aimed at increasing A. blood volume B. degree of myocardial depression C. heart rate D. myocardial contractility E. vasoconstriction |
E. vasoconstriction
see wiki discussion. Maintain: • Sinus Rhythm • Slow Rate • Full Preload • Normal / Low Contractility • High Afterload ----------- |
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MC119
The medical therapy for unstable angina which is most effective in reducing progression to myocardial infarction is A. aspirin B. beta-blockers C. calcium channel blockers D. glyceral trinitrate E. thrombolytic therapy |
A. Aspirin
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MC121
Correct statements regarding atrial fibrillation include all of the following EXCEPT A. A history of hypertension, associated with atrial fibrillation, increases stroke risk. B. A history of poor left ventricular systolic function, associated with atrial fibrillation, increases stroke risk. C. Anticoagulation should be continued for one month following successful cardioversion of atrial fibrillation. D. Anticoagulation therapy (to an INR of 2.0) decreases the risk of stroke by up to 50%. E. Atrial fibrillation becomes an increasingly important cause of stroke with advancing age. |
D. Anticoagulation therapy (to an INR of 2.0) decreases the risk of stroke by up to 50%.
Indications for antithrombotic therapy with warfarin (target INR of 2 to 3) == • Patients aged over 75 • Patients with a history of thromboembolic disease • Patients with hypertension, thyrotoxicosis or other risk factors* • In patients aged over 60 with coronary artery disease or diabetes mellitus, low dose aspirin is recommended alongside warfarin *Risk factors for thromboembolism include heart failure, ejection fraction <35%, hypertension, diabetes mellitus Anticoagulation == ==== A meta-analysis of 16 trials of antithrombotic strategies concluded that dose-adjusted oral anticoagulation was highly effective at preventing stroke (both ischaemic and haemorrhagic) in patients with AF with a relative risk reduction of 61% (Figure 5). Close monitoring of the international normalized ratio (INR) is essential, particularly if the patient is undergoing cardioversion, as the risk of stroke increases considerably if the INR drops below 1.7. Aspirin reduces the stroke risk by just 22%. The Seventh American Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy has recommended adding aspirin (75 mg) to warfarin in patients with AF and atherosclerosis to prevent ischaemic coronary events. In patients undergoing either electrical or pharmacological cardioversion of AF it is generally accepted that anticoagulation therapy is not essential if the episode has lasted less than 48 hours. If in doubt, transoesophageal echocardiography can be performed to exclude left atrial appendage thrombus. |
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MC122
In a patient with aortic stenosis, A. aortic regurgitation is rarely seen B. loss of sinus rhythm is poorly tolerated C. presentation is usually with a cerebrovascular accident D. the characteristic compensation of the left ventricle is dilatation E. the most common aetiology is rheumatic calcification |
B. loss of sinus rhythm is poorly tolerated
----------- The most common forms of aortic valve disease include: (1) congenital aortic stenosis, usually resulting from failure of the valve commissures to develop fully, often resulting in unicuspid aortic valves, (2) degenerative changes in a congenitally bicuspid aortic valve, and (3) athero-calcific disease in a trileaflet aortic valve.http:// clevelandclinicmeded.com/diseasemanagement/cardiology/aortic_valve/aortic_valve.htm |
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MC123
The first heart sound on auscultation is A. characteristically quiet in mitral stenosis B. due equally to mitral and tricuspid valve closure C. louder than usual with a premature beat D. loudest at the left sternal edge E. unchanged in mitral regurgitation |
C. louder than usual with a premature beat
~~ Loud S1 with: • MS & TS (valve cusps widely apart at the onset of systole ie. cusps remain mobile) • Tachycardia (shortened diastolic filling time) Soft S1 with: • 1st degree HB - prolonged diastolic filling time • LBBB - delayed onset of LV systole • MR - failure of lealets to coapt normally It is produced mainly by mitral valve closure and, to a lesser extent, by tricuspid valve closure. Heard best it apex. ----------- MEDICINE 34:4 - Clinical examination of the heart (Brian Kirby, Kenneth MacLeod) First heart sound: S1 marks the onset of systole. It is produced mainly by mitral valve closure and, to a lesser extent, by tricuspid valve closure. Timing of the heart sounds is aided by gently palpating the carotid pulse with the fingers of the left hand while moving the stethoscope, as described above, with the right hand.The intensity of S1 varies with the position of the valve cusps at the onset of ventricular contraction. Their position is determined by the volume and pressure of blood on either side of the valve; the wider apart the cusps at the onset of systole, the louder the sound produced. Thus, any change in cusp position at the onset of systole affects the sound produced; it varies with, for example: • P–R interval • rate of valve closure • valve mobility • force of ventricular systole. Splitting of S1 results from asynchrony of right and left heart systole as a consequence of conduction abnormalities (e.g. right bundle branch block, LV pacing, LV ectopic rhythms) or mechanical causes (e.g atrial septal defect, tricuspid stenosis, Ebstein’s anomaly). |
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MC124
Each of the following statments regarding DVIR pacing is true EXCEPT A. atrial sensing inhibits atrial pacing B. pacing will usually provide AV (atrioventricualr) synchrony C. the rate of pacing can be altered by patient activity D. ventricular sensing inhibits ventricular pacing E. ventricular sensing inhibits atrial pacing |
A. atrial sensing inhibits atrial pacing (false so answer to choose)
• D - Dual Chamber Pacing • V - Ventricle Sensed • I - Inhibits when sensed • R - Rate Modulation ----------- |
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MC125
In a patient with aortic stenosis, A. aortic regurgitation is rarely seen B. the characteristic compensation of the left ventricle is dilatation C. presentation is usually with a cerebrovascular accident D. a valve area of < 0.8 cm2 represents severe disease E. atrial arrhythmias are commonly seen |
D. a valve area of < 0.8 cm2 represents severe disease
Severe AS - AVA < 1.0cm2 • usually coexisting AR • characteristic compensation is LVH • usually present with dyspnoea, angina or syncope • associated arrhythmias uncommon ----------- |
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MC126 ANZCA version [2002-Mar] Q135 [2010- August] Q66
Left ventricular diastolic dysfunction 1. can be diagnosed with transoesophageal echocardiography. 2. is improved by propofol anaesthesia. 3. is suggested by an early to late (atrial) mitral inflow velocity ratio (E/A) of less than one 4. following an old myocardial infarction is mainly due to delayed ventricular relaxation |
1. can be diagnosed with transoesophageal echocardiography.
3. is suggested by an early to late (atrial) mitral inflow velocity ratio (E/A) of less than one ----------- 1. True 2. False 3. True. With diastolic dysfunction, during diastole the LV is unable to relax normally due to inadequate uptake of Ca intracellularly. Note that this is an energy dependent process and proceeds less well in damaged or ischaemic (stunned) myocardium. Hence during diastole, LV pressure is higher than normal. The result of this is that there is a reduced pressure gradient across the mitral valve during diastole from emptying of the RV. Hence the E peak velocity is reduced. The A wave remains the same as atrial contraction is normally not impaired. Hence the E-A ratio is decreased. 4. False. ?This can lead to impaired diastolic function but couldn't find a reference for delayed relaxation I think old MI gives fibrosis. |
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MC127
A 28 yr old patient with hypertrophic obstructive cardiomyopathy (HOCM) presents for an emergency laparotomy for suspected ectopic pregnancy. In anaesthetising this patient it is important to A. maintain a pulse rate of at least 100 beats.min-1 B. increase cardiac contractility C. reduce preload D. maintain sinus rhythm |
D. maintain sinus rhythm
• Sinus Rhythm • Slow Rate • Full Preload • Normal / Low Contractility • High Afterload ----------- |
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MC128
The normal range of the QRS axis in the ECG is A. 0 to +I80 degrees B. 0 to +90 degrees C. -30 to +90 degrees D. -90 to +90 degrees E. -90 to +30 degrees |
B. -30 to 90C. -30 to +90 degrees
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MC129
In providing general anaesthesia for patients with congenital long QT syndromes, which of the following statements is correct? A. a priming dose of a non-depolarising muscle relaxant protects against succinylcholine induced arrhythmias B. beta-blocking drugs are relatively contra-indicated C. low dose droperidol is safe D. pre-induction infusion of magnesium sulphate should NOT be used E. thiopentone leaves the QT interval unchanged |
A. a priming dose of a non-depolarising muscle relaxant protects against succinylcholine induced arrhythmias
Good review article Anesthesia for patients with congenital long QT syndrome. Anesthesiology. 2005 Jan;102(1):204-10 From article, B, C, D, E definitely incorrect. "The ideal muscle relaxant should avoid bradycardia, vagal stimulation, and potassium shifts. It should have little or no histamine release and be short acting to avoid the use of reversal agents. Accordingly, succinylcholine, because of its autonomic effects and potassium release, is far from ideal. It prolongs the QT interval in patients with c-LQTS unless pretreatment with a priming dose of tubocurarine is used." ----------- |
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MC130
A patient with known ischaemic heart disease undergoes percutaneous coronary artery stenting (with a non drug-eluting stent) prior to major elective surgery. Ideally the surgery should be postponed for A. 1-4 weeks B. 4-8 weeks C. 8-12 weeks D. 12-24 weeks E. over 24 weeks |
B. 4-8 weeks
ACC/AHA Guideline Update on Perioperative Cardiovascular Evaluation for Noncardiac Surgery (2002) Given that stent thrombosis remains a very morbid event, resulting in Q-wave MI or death in the majority of patients in whom it occurs, and given that the risk of stent thrombosis diminishes after endothelialization of the stent has occurred (which generally takes 4 to 8 weeks), it appears reasonable to delay elective noncardiac surgery for 2 weeks and ideally 4 weeks to allow for at least partial endothelialization of the stent, but not for more than 6 weeks or 8 weeks, when restenosis begins to occur (if it is to occur). ----------- |
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MC131
The cardiac valvular lesion identified as the MOST significant risk factor for non-cardiac surgery is severe A. aortic incompetence B. aortic stenosis C. mitral incompetence D. mitral stenosis E. tricuspid incompetence |
B. aortic stenosis
• From ACC/AHA Guideline Update on Perioperative Cardiovascular Evaluation for Noncardiac Surgery (http://www.acc.org/clinical/guidelines/perio/clean/perio_index.htm) "Severe aortic stenosis poses the greatest risk for noncardiac surgery. If the aortic stenosis is severe and symptomatic, elective noncardiac surgery should generally be postponed or canceled. Such patients require aortic valve replacement before elective but necessary noncardiac surgery. On the other hand, in patients with severe aortic stenosis who refuse cardiac surgery or are otherwise not candidates for aortic valve replacement, noncardiac surgery can be performed with a mortality risk of approximately 10%. In rare instances, percutaneous balloon aortic valvuloplasty may be justified when the patient is not a candidate for valve replacement." ----------- |
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MC132
Ischaemic preconditioning limits myocardial damage during subsequent ischaemic insult. This process is inhibited by A. alpha-2 agonists B. insulin C. isoflurane D. opioids E. sulfonylureas |
E. sulfonylureas
~~ • Cardiac preconditioning is thought to be due to action of ATP K+ channels. • These are typically blocked by sulphonylureas. ----------- Cardiac preconditioning represents the most potent and consistently reproducible method of rescuing heart tissue from undergoing irreversible ischaemic damage. Major milestones regarding the elucidation of this phenomenon have been passed in the last two decades. The signalling and amplification cascades from the preconditioning stimulus, be it ischaemic or pharmacological, to the putative end-effectors, including the mechanisms involved in cellular protection, are discussed in this review. Volatile anaesthetics and opioids effectively elicit pharmacological preconditioning. Anaesthetic-induced preconditioning and ischaemic preconditioning share many fundamental steps, including activation of G-protein-coupled receptors, multiple protein kinases and ATP-sensitive potassium channels (K-ATP channels). Volatile anaesthetics prime the activation of the sarcolemmal and mitochondrial K-ATP channels, the putative end-effectors of preconditioning, by stimulation of adenosine receptors and subsequent activation of protein kinase C (PKC) and by increased formation of nitric oxide and free oxygen radicals. In the case of desflurane, stimulation of α- and β-adrenergic receptors may also be of importance. Similarly, opioids activate δ- and κ-opioid receptors, and this also leads to PKC activation. Activated PKC acts as an amplifier of the preconditioning stimulus and stabilizes, by phosphorylation, the open state of the mitochondrial K-ATP channel (the main end-effector in anaesthetic preconditioning) and the sarcolemmal K-ATP channel. The opening of K-ATP channels ultimately elicits cytoprotection by decreasing cytosolic and mitochondrial Ca2+ overload. -from Br J Anaesth 2003; 91: 551–65 |
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MC133
When assessing a patient with unstable angina, the clinical feature most predictive of an adverse short-term outcome (death or myocardial infarction within 6 months) is A. Increased angina frequency or severity B. Angina provoked at a lower threshold of exercise C. New onset angina on effort D. An angina episode lasting more than 10 minutes E. Age less than 65 years |
A. Increased angina frequency or severity
ACC/AHA 2002 Guideline Update for the Management of Patients With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction ----------- |
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MC134
Correct statements regarding Hypertrophic Cardiomyopathy include each of the following EXCEPT that it A. results in a left ventricular wall thickness of greater than 12 mm B. is a condition where the left ventricle is hypertrophied and dilated C. is predominantly a non-obstructive disease D. is most easily and reliably diagnosed with 2- dimensional echocardiography E. the hypertrophy is characteristically asymmetrical |
B. is a condition where the left ventricle is hypertrophied and dilated
(not dilated) Congenital Hypertrophic Cardiomyopathy == • Autosomal dominant genetic disorder • Ventricular wall usually ≥ 15mm (may be normal in some variants of HCM) • Results in hypertrophic ventricle (symmetrical and asymmetrical) • Does not usually result in outflow obstruction • Can be assessed by 2D or 3D echo or MRI • Sudden death due to arrhythmias |
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MC135 (black bank version)
You are called to the cardiac catheter lab to assist. A patient having a difficult right coronary stent has become agitated. On arrival his GCS is 15, is talking but sweaty, SaO2 97% heart rate is 60, blood pressure 80/60 with marked reduction in the invasive arterial blood pressure trace on inspiration, CVP +2. What is your next action? A. Intubate and ventilate B. transfer to theatre immediately C. Quick transthoracic echo D. start adrenaline infusion E. give atropine |
C. Quick transthoracic echo
• Would diagnose/exclude tamponade and give an allow assessment of EF. No indication to I&V, May need to go to OT but need a diagnosis first. Differential diagnosis: • Tamponade secondary to RCA rupture • Cardiogenic shock due to infarction or ischaemia • Hypovolaemic shock - Diuretic overdose - Occult haemorrhage • Anaphylaxis (rare, but would explain low CVP and tachycardia may be blocked by betablockers) • Drug error ----------- |
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MC136
During controlled ventilation of a neonate prior to repair of a truncus arteriosus which of the following is MOST likely to be deleterious? A. controlled hypoventilation B. ventilation with air C. ventilation with an FiO2 of 0.18 D. ventilation with nitric oxide E. ventilation with PEEP of 3 cmHO |
D. ventilation with nitric oxide
Principle: Maintain High PVR to ensure that blood is directed systemically • Low FiO2, Acidosis, Hypercarbia, Sympothomimetics, High positive end-expiratory pressure TRUNCUS ARTERIOSUS (TA) is an uncommon congenital cardiovascular anomaly that is characterized by a single arterial trunk arising from the normally formed ventricles by means of a single semilunar valve (ie, truncal valve). In addition, the pulmonary arteries originate from the common arterial trunk distal to the coronary arteries and proximal to the first brachiocephalic branch of the aortic arch. The common trunk typically straddles a defect in the outlet portion of the interventricular septum (ie, conal septum); however, in rare cases, it may originate almost completely from the right or left ventricle. In patients with a patent and normal caliber aortic arch, the ductus arteriosus is either absent or diminutive. ----------- |
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MC137
A common finding in hereditary prolonged QT syndrome is: A. bifid T waves B. inverted P waves C. prolonged QRS complex D. R axis deviation E. short PR interval |
A. bifid T waves
"T wave and U wave abnormalities are common in LQTS. T waves may be larger, prolonged, or have a notched, bifid or biphasic appearance. A pathognomonic feature of LQTS is so-called T wave alternans, where there is beat-tobeat variation in T wave amplitude" (BJA 2003; 90(3): 349-66) ----------- |
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MC138
Ebstein's anomaly is an abnormality of A. Aortic valve B. Mitral valve C. Pulmonary valve D. Pulmonary veins E. Tricuspid valve |
E. Tricuspid valve
Ebstein anomaly is a congenital malformation of the heart that is characterized by apical displacement of the septal and posterior tricuspid valve leaflets, leading to atrialization of the right ventricle with a variable degree of malformation and displacement of the anterior leaflet http://www.emedicine.com/med/topic627.htm ----------- |
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MC139 ANZCA Version [Jul06][Apr07]
A diagnosis of pulmonary embolism is most strongly suggested by A. intraluminal filling defects or vascular cutoffs on angiography B. PaO2 less than 85 mmHg and an abnormal lung perfusion scan C. PaO2 less than 85 mmHg and an elevated PaCOz D. right ventricular hypertrophy with right ventricular strain and right axis deviation on electrocardiography E. "unmatched" ventilation-perfusion defects |
A. intraluminal filling defects or vascular cutoffs on angiography
----------- MEDICINE 2002: Pulmonary Embolism and Venous Thrombosis (Michael D Stewart, Huon H Gray) Investigations === ECG changes (Figure 4) are generally nonspecific and may include sinus tachycardia, atrial fibrillation and T wave changes with ST segment abnormalities, particularly in the anteroseptal leads (V1–V3). Some ECG changes are present in 87% of patients with proven PE and without pre-existing cardiopulmonary disease. Characteristic abnormalities (including the S1, Q3, T3 pattern, right bundle branch block, P pulmonale and right-axis deviation) are less common (30% of patients with massive PE). ECHOCARDIOGRAPHY may be useful in the differential diagnosis of acute dyspnoea and chest pain in patients with no previous cardiorespiratory disease. RV dysfunction often accompanies massive PE and is associated with a higher mortality; RV ischaemia, ultimately leading to biventricular failure, is the principal cause of death in patients who succumb to acute PE. Right heart dilatation is not diagnostic but may support the diagnosis of acute PE, and estimation of RV pressure may be possible if tricuspid regurgitation is detected. Changes in RV pressure may also be used as a guide to the effectiveness of thrombolytic therapy, or as an indicator of the progression of chronic pulmonary hypertension. Occasionally, thrombus is seen in the right heart, and transoesophageal echocardiography may identify thrombus in the main pulmonary artery. If a patent foramen ovale or atrial septal defect is seen, special consideration must be given to the management of potential paradoxical embolism from the venous to the systemic circulation. CHEST RADIOGRAPH changes are common but nonspecific, and include atelectasis, pleural effusion, pulmonary infiltrates and elevation of a hemidiaphragm. Dilatation of a major proximal pulmonary artery and areas of pulmonary oligaemia may suggest major arterial obstruction. Wedge-shaped opacities in the peripheral lung fields, caused by pulmonary infarction, may be seen in patients with minor PE. In chronic thromboembolic pulmonary hypertension, the cardiothoracic ratio may be increased and there may be features suggesting RV dilatation, patchy oligaemia and dilatation of the main pulmonary arteries. In patients with suspected PE, the chest radiograph is more helpful when it suggests alternative diagnoses such as pneumonia or pneumothorax. ISOTOPE RADIONUCLIDE ventilation–perfusion (V/Q) lung scanning (Figure 5) remains the principal investigation in suspected PE; a normal scan excludes clinically signifi cant PE. However, abnormal perfusion occurs in conditions other than PE (e.g. chronic lung disease, pneumonia), and when ventilation is assessed simultaneously, evidence of V/Q mismatch greatly increases the likelihood that PE is the cause of reduced perfusion. The clinical likelihood of PE is taken into account when interpreting the radionuclide scan, the result of which is usually reported as representing a low, intermediate or high probability of PE. However, interpretation may be inconclusive because of the disparity between the clinical and V/Q scan likelihood of PE; for example, when the clinical suspicion is high, 40% of patients with a low-probability V/Q scan are found to have PE on further examination. Nevertheless, patients in whom the isotope perfusion scan is normal are extremely unlikely to have PE. The diagnosis of PE can be considered confirmed when the index of clinical suspicion is high and the isotope scan suggests that PE is highly likely. When suggestive of PE, radionuclide scanning tends to underestimate the angiographic severity and haemodynamic disturbance of PE. CT AND MRI are increasingly used to investigate suspected PE, particularly in patients with pre-existing cardiopulmonary disease. Following a bolus injection of contrast, a CT pulmonary angiogram can be obtained and emboli within the pulmonary arteries can be directly visualized down to the subsegmental vessel. Spiral CT angiography identifi es emboli in the main, lobar and segmental pulmonary arteries, but cannot exclude emboli beyond the subsegmental level. Right heart size can be assessed and coexistent pathology (e.g. aortic dissection) may be detected. PULMONARY ANGIOGRAPHY remains the definitive investigation in confi rming the presence of PE. It should be considered in patients in whom clinical suspicion is high who have undergone non-diagnostic radionuclide scanning or CT, and in patients at considerable risk from long-term anticoagulation (e.g. following neurosurgery), in whom the diagnosis of PE must be made with an even greater degree of certainty. D-DIMER – in conditions in which thrombus is formed, plasmin-mediated proteolysis of cross-linked fi brin releases D-dimeric fragments. Increased levels of D-dimer (assayed by a quantitative enzyme-linked immunosorbent assay (ELISA) or an ELISA-derived method) can be identifi ed in 99% of patients with PE proved by V/Q lung scanning. However, though elevated D-dimer levels are sensitive for the presence of PE, they are not specifi c. Levels are also elevated for up to 1 week postoperatively, in myocardial infarction (MI), in malignancy, and in sepsis and other systemic illnesses. A negative test may therefore support a low clinical suspicion of PE, but a positive test cannot be used to make a diagnosis of VTE. D-dimer assay may become useful in reducing the number of radionuclide scans undertaken in patients in whom the clinical suspicion of PE is low. |
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MC140
Regarding a 75-year-old female patient with moderate aortic stenosis presenting for an elective hip replacement, A. atrial systole has an increased contribution to stroke volume (compared to a patient with no aortic stenosis) B. beta-blockers are poorly tolerated in this degree of aortic stenosis C. hypotension is better tolerated than hypertension D. rheumatic heart disease is the commonest aetiology in this age group in Western Society E. spinal anaesthesia is the preferred method of anaesthesia |
A. atrial systole has an increased contribution to stroke volume (compared to a patient with no aortic stenosis)
"The hypertrophied ventricle becomes increasingly stiff, causing diastolic dysfunction with a reduced compliance. Consequently, left ventricular filling becomes dependent on atrial contraction with atrial systole contributing 40%, instead of the usual 20%, of left ventricular end-diastolic volume. The left atrium hypertrophies to maintain left ventricular filling. Preservation of sinus rhythm becomes vital for the maintenance of cardiac output." B. beta-blockers are poorly tolerated in this degree of aortic stenosis - false C. hypotension is better tolerated than hypertension - false: "Avoidance of systemic hypotension is essential" D. rheumatic heart disease is the commonest aetiology in this age group in Western Society - false: "Isolated aortic stenosis, without coexisting mitral valve disease, is more common in males than females and is rarely rheumatic in origin." E. single shot spinal anaesthesia is the preferred method of anaesthesia - false: "Anaesthetic techniques that reduce systemic vascular resistance (e.g. regional neuroaxial techniques) must be used with extreme caution although successful cases of carefully titrated epidural and spinal blocks using catheters have been reported." ----------- |
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MC141
Atrial fibrillation: A. Rhythm control not proven to be better then rate control B. Only need warfarin if have other risk factors for CVA C. Aspirin is as good as warfarin for CVA protection in elderly D. After cardioversion patient should be placed on rhythm control therapy E. Digoxin is the drug of choice for rate control in exercise |
A. rhythm control not proven to be better then rate control
~~ NB this is remembered version ----------- MEDICINE 34:7 - ATRIAL FIBRILLATION (Andrew R J Mitchell) Rhythm vs Rate Control: === Rhythm control Publication of the AFFIRM and RACE studies in 2002 indicated that in elderly asymptomatic patients with AF there was no quality of life or survival advantage in trying to restore and maintain sinus rhythm. These studies also suggested that anticoagulant therapy should not be stopped soon after cardioversion as the first re-presentation with AF may be with stroke. Cardioversion, however, still has a role in younger symptomatic patients. Additionally, in patients with mild-to-moderate heart failure, restoration and maintenance of sinus rhythm has beneficial long-term effects on left ventricular function and survival. Rate control If patients are managed in permanent AF then ventricular rate control can be obtained with beta-blockers, calcium antagonists (particularly diltiazem or verapamil) and digoxin. The AFFIRM rate control substudy has shown that adequate rate control (defined as a resting heart rate of less than 80 bpm and an average heart rate of <100 bpm on 24-hour ambulatory monitoring) is best (70% of patients) achieved by the use of a beta-blocker with or without digoxin. This compares with adequate control in 54% of patients with calcium-channel blockers (with or without digoxin) and 58% of patients with digoxin alone. Amiodarone is not usually recommended for rate control in permanent AF but is moderately effective when given intravenously for rate control in acute AF. If permanent AF is accepted, then antithrombotic therapy should be continued. Indications for antithrombotic therapy with warfarin (target INR of 2 to 3) == • Patients aged over 75 • Patients with a history of thromboembolic disease • Patients with hypertension, thyrotoxicosis or other risk factors* • In patients aged over 60 with coronary artery disease or diabetes mellitus, low dose aspirin is recommended alongside warfarin *Risk factors for thromboembolism include heart failure, ejection fraction <35%, hypertension, diabetes mellitus Anticoagulation ==== A meta-analysis of 16 trials of antithrombotic strategies concluded that dose-adjusted oral anticoagulation was highly effective at preventing stroke (both ischaemic and haemorrhagic) in patients with AF with a relative risk reduction of 61% (Figure 5). Close monitoring of the international normalized ratio (INR) is essential, particularly if the patient is undergoing cardioversion, as the risk of stroke increases considerably if the INR drops below 1.7. Aspirin reduces the stroke risk by just 22%. The Seventh American Chest Physicians Conference on Antithrombotic and Thrombolytic Therapy has recommended adding aspirin (75 mg) to warfarin in patients with AF and atherosclerosis to prevent ischaemic coronary events. In patients undergoing either electrical or pharmacological cardioversion of AF it is generally accepted that anticoagulation therapy is not essential if the episode has lasted less than 48 hours. If in doubt, transoesophageal echocardiography can be performed to exclude left atrial appendage thrombus. Electrical Cardioversion == Electrical direct current cardioversion of persistent AF remains the most effective method of restoring sinus rhythm. Over 80% of episodes can be terminated with modern biphasic defibrillators. Pre-treatment of patients with anti-arrhythmic drug therapy will improve the likelihood of restoring and maintaining sinus rhythm at one year from just 25% to over 60% (with amiodarone). Cardioversion is best achieved using high starting energies (360J monophasic, 200J biphasic), an antero-posterior shock configuration and firm manual pressure to the paddles. If external cardioversion of persistent AF fails then patients can be considered for internal cardioversion (effective in over 90% of patients who were previously resistant to external cardioversion) |
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MC142
The following statements regarding prolonged QT syndrome are true EXCEPT A. all patients with the syndrome have a prolonged QTc (QT interval corrected for heart rate) B. a QTc greater than 500 msec is considered prolonged C. exercise testing may provoke a prolongation of the QTc D. T and U wave abnormalities are common E. T wave alternans is pathognomonic of the syndrome |
A. all patients with the syndrome have a prolonged QTc (QT interval corrected for heart rate) - false so answer to choose.
Straight from "Long QT syndrome and anaesthesia" (PD Booker, SD Whyte and EJ Ladusans) * A - False (therefore answer) --> "6% of patients with symptomatic LQTS have a normal QTc interval." * B - True --> "QTc interval of >440 ms is considered prolonged", therefore > 500 msec is definitely prolonged * C - True --> "Exercise testing of patients with LQTS may provoke prolongation of the QTc" * D - True --> "T wave and U wave abnormalities are common in LQTS" * E - True --> "A pathognomonic feature of LQTS is so-called T wave alternans, where there is beat-to-beat variation in T wave amplitude." ----------- |
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MC143 ANZCA version [2003-Aug] Q138, [2004-Apr] Q37, [2005-Sep] Q14, [Jul07], [Apr08]
This ECG (Lead V5) most likely represents A. Wolff-Parkinson-White (WPW) syndrome B. atrial fibrillation C. complete heart block D. atrio-ventricular junctional rhythm E. sinoatrial block |
D. atrio-ventricular junctional rhythm
Regular rate -> so not AF B Rate 75/min -> too fast for complete heart block - so not C No delta wave (so not WPW (option A)) Narrow QRS -> Supraventricular rhythm PLUS (no P wave before QRS) ->AV junctional rhythm (D) Retrograde P wave is predominantly negative and appears just after the QRS. I think the p wave is after the QRS ie retrograde P wave as seen in nodal (junctional) rhythm. ----------- |
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MC144
Early features of pulmonary hypertension include each of the following EXCEPT A. a narrowly split second heart sound (S2) B. an early diastolic murmur C. decreased oxygen saturation D. dyspnoea on exertion E. hyperlucent lung periphery on chest Xray |
B. an early diastolic murmur
The classic murmur of Pulm HT is the Graham-Steele murmur - a DIASTOLIC murmur audible along the left sternal border due to functional incompetence of the pulmonary valve in patients with pulmonary hypertension. The Graham-Steel murmur is a high-pitched, decrescendo murmur, loudest during inspiration. (RIGHT MURMURS LOUD ON INSPIRATION) -- detected with severe HT (late sign) ----------- A – True From UpToDate The initial physical finding of PH is usually increased intensity of the pulmonic component of the second heart sound, which may even become palpable. The second heart sound is narrowly split or single in patients with PH and preserved right ventricular function. Splitting of the second heart sound widens as the right ventricle fails or if right bundle branch block develops. B – Most False – only true in late disease - From UpToDate Auscultation of the heart may also reveal a systolic ejection murmur and, in more severe disease, a diastolic pulmonic regurgitation murmur. The right sided murmurs and gallops are augmented with inspiration. C – True Stoelting p131 Arterial hypoxaemia is almost always present, reflecting ventilation to perfusion imbalance due to increased perfusion of poorly ventilated alveoli, mixed venous hypoxaemia due to depression of the cardiac output, and shunting of blood through a patent foramen ovale D – True Stoelting p131 Dyspnoea is the most common reason for seeking medical attention There is a correlation between the distance walked during a 6 minute walk test and the severity of pulmonary hypertension E – True From UpToDate The characteristic chest radiograph shows enlargement of the central pulmonary arteries with attenuation of the peripheral vessels, resulting in oligemic lung fields |
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MC145
Each of the following are causes of right axis deviation on the ECG (electrocardiogram) EXCEPT A. chronic lung disease B. lateral myocardial infarction C. left anterior hemiblock D. left posterior hemiblock E. right ventricular hypertrophy |
C. left anterior hemiblock
Conditions associated with right axis deviation * Right ventricular hypertrophy * Left posterior hemiblock * Lateral myocardial infarction * Acute right heart strain ----------- Answer is C Conditions associated with right axis deviation Right ventricular hypertrophy Left posterior hemiblock Lateral myocardial infarction Acute right heart strain Incomplete left bundle branch block occurs in 2 forms, each called hemiblock. In left anterior hemiblock (LAH), transmission of the electrical impulse proceeds normally along the main left bundle branch and the posterior fascicle, but it is blocked or delayed in the anterior fascicle. This blockage results in delayed activation of the anterior portion of the left ventricle. In LAH, the duration of the QRS complex may be of normal or only slightly prolonged duration because of normal rapid conduction down the right and left main bundle and the left posterior fascicle. In addition, the QRS complex is directed superiorly in the frontal plane. This is called left axis deviation, although the term superior axis deviation most accurately describes the finding. Furthermore, QRS axis is normally to the left; therefore, the term left axis deviation makes little semantic sense. With left posterior hemiblock, transmission of the electrical impulse proceeds normally along the main left bundle branch and the anterior fascicle, but it is blocked in the posterior fascicle. This blockage results in delayed activation of the posterior left ventricle. The QRS complex is again of normal or only slightly prolonged duration and inscribes a rightward axis in the frontal plane. Left posterior hemiblock is rarely observed in children, and diagnosis is difficult because of the common association of right axis deviation in children with congenital heart disease and right ventricular hypertrophy.[1] - Agree answer C |
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MC146 [Sep05] [Apr07]
In the diagnosis of postoperative myocardial infarction A. echocardiography has little role to play B. infarct size can be judged from cumulative enzyme release C. new left bundle branch block on ECG confirms acute infarction D. serum troponins have high sensitivity and are detectable for up to 5 days E. ST segment elevation is extremely common |
D. serum troponins have high sensitivity and are detectable for up to 5 days
New LBBB is suggestive but does not confirm in absence of troponins. Read "Universal Definition of Myocardial Infarction". ----------- |
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MC147 [Sep05][Apr08][Oct08]
The diagram below is of a transgastric short axis view obtained during a transoesophageal echocardiography examination. Which letter corresponds to the area supplied by the right coronary artery? A. A B. B C. C D. D E. E http://www.anesthesia-analgesia.org/content/89/4/870/F5.large.jpg |
A. A
The LV short axis view at the level of the papillary muscles (TG Mid SAX) RCA - Blue LAD - Green Cx - Red IVS = intraventricular septum IW = inferior wall PW = posterior wall AW = anterior wall ----------- |
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MC148 [Mar06]
The most useful finding to confirm the diagnosis of aortic stenosis in an adult with a systolic murmur is A. increasing murmur intensity with inspiration B. decreasing murmur intensity with passive leg elevation C. increased second heart sound D. effort syncope E. a slow rate of rise of the carotid pulse |
D. effort syncope (can also occur with HOCM)
E. a slow rate of rise of the carotid pulse (can also occur normally in elderly with diseased arteries) ➮ soft S2 ➮ left sided murmurs louder on expiration R sided murmurs increased with inspiration (increased venous return to R side of heart), L sided murmurs (incl AS) decreased with insp. (RILE) ----------- |
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MC149 ANZCA Version [Apr07][Jul07][Mar10][Mar11][Sep11][Mar12]
Reverse splitting of the 2nd heart sound is caused by A. acute pulmonary embolism B. ASD C. complete LBBB D. severe MR E. pulmonary HT |
C. LBBB
(and severe AS). Usually the LEFT side closes first (ie Aortic then pulmonary) - this is because the left sided contraction starts first Fixed splitting in ASD - ie the usual widening on inspiration (due to late P2) is lost. Paradoxical splitting of S2 occurs when the aortic valve closes after the pulmonic valve, and P2 is heard before A2. Seen when there is delayed activation of the left ventricle (LBBB, RV Pacemaker) or decreased LV outflow (aortic stenosis, HOCM) ----------- In most healthy adults, a splitting of S2 can be heard during deep inspiration. The reason for this relates to the fact mentioned in the murmur overview discussion that the second heart sound is actually a blending of the closing sounds of two distinct heart valves. Normally, the aortic valve closes just before the pulmonary valve, but they are so close together that the sound is a uniform and instantaneous S2. When a person takes in a deep breath, the decrease in intrathoracic pressure causes an increase in venous return. This causes the right atrium and ventricle to fill slightly more than normal, and it takes the ventricle slightly longer during systole to eject this extra blood. This delay in ejection forces the pulmonary valve to stay open a bit longer than usual, and the normally small difference between aortic and pulmonary valve closure becomes noticeable as a split S2. |
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MC151
All of the following prolong the QT interval except A. Increased airway pressures B. Suxamethonium C. Magnesium D. Volatile anaesthetics E. Thiopentone |
C. MgSO4 does not prolong the QTI, it is treatment for Torsades (30mg/kg).
Sux, vol's and Barb's all prolong QTI. (Anaesthesiology 2005; 102:204-10) Related MC142 Presumably high airway pressures increase QTI via increased sympathetic stimln. ----------- |
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MC151 ANZCA Version [Apr07][Mar10][Sep11][Mar12]
All of the following prolong the QT interval except A. high intra-thoracic pressure B. hypothermia C. magnesium sulphate D. suxamethonium E. volatile anaesthetic agents |
C. Magnesium
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MC152
60 y.o with acute aortic regurgitation. In pulmonary oedema. BP 160/90. HR was about 90. What is the best treatment pre-op: A. Intra aortic balloon pump B. Dobutamine infusion C. Sodium nitroprusside infusion D. Beta blocker E. Dopamine infusion |
C. Sodium nitroprusside infusion
vasodilators in the context of hypertension rather than inotropy From UptoDate, Acute aortic regurgitation: "The treatment of acute severe AR is emergency aortic valve replacement. If there is any delay in surgery, stabilization may be attempted in the intensive care unit using intravenous vasodilators, such as nitroprusside, and possibly inotropic agents such as dopamine or dobutamine in an attempt to enhance forward flow and lower left ventricular end-diastolic pressure [7]. An intraaortic balloon pump is contraindicated because inflation of the balloon in diastole will worsen the severity of AR." ----------- see wiki debate. Official version had acute aortic regurg secondary to ascending aortic dissection. If this was the case then b-blocker, but if AR alone, SNP. |
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MC153 [Jul07]
CVP changes: A. a wave increases with atrial fibrillation B. x and y descents are decreased with constrictive pericarditis C. get sigmoid wave with lack of y descent with tamponade D. ?a and v waves reduced with extensive RV infarct E. trace becomes monophasic with obliteration of the y descent in tamponade F. steeper than usual x descent may suggest tricuspid regurgitation |
C. get sigmoid wave with lack of y descent with tamponade
"the CVP becomes monophasic and displays a single prominent x descent and an attenuated or absent y descent" Getting the most out of a CVP catheter - ASA Refresher ➭ In AF the a wave disappears, and the c wave becomes more prominent, since atrial volume is greater at end-diastole and onset of systole, owing to the absence of atrial contraction ➭ ----------- |
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MC153 [Jul07] ANZCA version
When viewing the central venous pressure trace: A. an accentuated "a" wave supports the diagnosis of atrial fibrillation B. a steeper than normal "x" descent supports the diagnosis of tricuspid regurgitation C. blunted "a" and "v" waves are associated with extensive right ventricular infarction D. flattened "x" and "y" descents are associated with pericardial constriction E. a monophasic pattern with obliteration of the "y" descent supports the diagnosis of pericardial tamponade |
E. a monophasic pattern with obliteration of the "y" descent supports the diagnosis of pericardial tamponade
----------- A - False In atrial fibrillation, a waves will be absent, and in atrioventricular dissociation, a waves will be dramatically increased ("cannon waves") as the atrium contracts against a closed tricuspid valve. B - False In tricuspid regurgitation, the c wave and x descent will be replaced by a large positive wave of regurgitation as the blood flows back into the right atrium during ventricular contraction C - False Prom a and v waves with RV infarction due to (a wave) increased atrial pressure from contraction into stiff RV (kind of like increased RA afterload) and v waves increased as often assoc TR hence increased filling RA. D - False Pericardial constriction – tall a and v waves, steep x and y descents |
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MC154 ANZCA version [Jul07] Q90
Clinical features supporting the diagnosis of cardiac tamponade include all of the following EXCEPT A. equal diastolic pressures of all heart chambers B. ST segment abnormalities C. increased venous pressure and cardiac output with fluid loading D. increased patient comfort in the sitting position E. impalpable apex beat and soft heart sounds |
All options can occur with tamponade.
?B. ST segment abnormalities as best answer - ST segment abnormalities may occur, though they don't so much support the diagnosis as fail to refute it. Can get electrical alternates with large effusions. ----------- |
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MC155 ANZCA version [Jul07] Q148
The LEAST desirable position for the tip of a central venous catheter which has been inserted into the left internal jugular vein is A. mid-way along the left brachiocephalic vein B. at the junction of the left brachiocephalic vein and the superior vena cava (SVC) C. in the SVC at the level of the carina D. at the junction of the SVC and the right atrium E. in the right atrium |
B. at junction brachiocephalic trunk and SVC
see wiki. "Left-sided catheters pose a particular problem because the left innominate (brachiocephalic) vein forms a near right angle to the SVC. Catheters entering the SVC from the left therefore have a tendency to impinge on the lateral wall of the SVC. The resulting increased risk of perforation is well documented" pref grp chose d??? which is actually the ideal position ----------- |
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MC156 ANZCA Version [Jul07][Apr08][Mar10]
Regarding patients aged 65 years or older with recurrent atrial fibrillation (AF) A. amiodarone and digoxin have similar efficacy in restoring sinus rhythm B. patients who have been reverted to sinus rhythm should still remain on warfarin therapy C. patients who remain in atrial fibrillation with heart rates less than 80 beats per minute do NOT require long term warfarin therapy D. peri-operative therapy with a beta-blocker will commonly lead to restoration of sinus rhythm E. restoration of sinus rhythm with electrical DC cardioversion improves long-term survival in comparison to controlling heart rate alone |
B. patients who have been reverted to sinus rhythm should still remain on warfarin therapy
- Wiki: Regards A: eTG does not rate digoxin as a cardioversion agent, solely for AV nodal blocking properties (ie as pre-treatment for flecainide or for rate control). So, FALSE. (Bip-bowww) Regards B: According to the eTG cardiovascular (2008 edition), a patient who undergoes cardioversion should at least remain on anticoagulative therapy for a short while after DC reversion because of the risk of atrial thrombus formation in the stunned atrium, even if a pre-revision echo shows no clot. However, if the patient is otherwise healthy and under the age of 55 this is 'commonly not done'. Long-term, "There is no consensus about duration of anticoagulation following successful cardioversion, but because many strokes occur soon after relapse into atrial fibrillation, it is possibly wise to continue warfarin whenever there is thought to be a reasonable risk of relapse (ie continue generally closer to 12 months)". Given the stem specifies patients over 65, I think this could be a reasonable answer. TRUE (-ish)(Ding!) Regards C: again, from the eTG "Reduction of thromboembolic complications is a major issue regardless of whether rate control or rhythm control is adopted as the primary 'antiarrhythmic' strategy. Atrial fibrillation itself rarely causes death or serious morbidity except through thromboembolic complications. All patients in whom atrial fibrillation is discovered, whether because of symptoms or as a chance finding (as is often the case in elderly patients), should be considered for long-term anticoagulation with warfarin. This will by no means always be the correct strategy for the individual patient, but the issue should be specifically considered, discussed with the patient, and reasons for not anticoagulating documented. A very recent report has highlighted the high risks of bleeding in the first year after starting warfarin in patients aged over 80 years, and the decision whether to commence warfarin or not is often a difficult one, especially as patients at higher risk of thromboembolism also tend to be those with risk factors for bleeding on warfarin." So that would mean C is FALSE - UNLESS they are over 80. perhaps.(Bip-bowww) Regards D: Sounds like baloney to me. FALSE (Although my dad swears he has been cardioverted by propofol alone). (sorry Dad: Bip-bowww) Regards E:, from eTG "a very large multinational study with over 4000 patients randomised to these treatment options for a mean of four years follow-up (the AFFIRM trial) [Note 1] showed no statistically significant difference in mortality or in quality of life between the two groups, with a trend favouring the rate control arm in terms of mortality. A more recent meta-analysis of this and similar smaller studies confirmed this view. However, trials such as AFFIRM are aimed largely at patients who have prolonged paroxysms of atrial fibrillation or persistent atrial fibrillation or atrial flutter, or patients whose chronic atrial fibrillation has been of reasonably recent onset, and therefore may not be directly applicable to patients with short-lived paroxysms of atrial fibrillation or patients with many years of chronic atrial fibrillation.... "The results of AFFIRM indicate that there is no imperative to attempt cardioversion with patients who tolerate atrial fibrillation well, although at least some studies suggest quality of life may be improved by being in sinus rhythm". So this option sounds like pork pies too. FALSE (Bip-bowww) |
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MC157 [Mar10][Aug10][Mar11] [Sep11]
An 18 yo with Fontan Circulation undergoing exploratory laparotomy. On ICU vent, sats 70%. Which ventilator parameter would you INCREASE to improve his sats? A. Bilevel pressure B. Expiratory time C. Inspiratory time D. Peak inspiratory pressure E. PEEP |
B. Expiratory time
Increase expiratory time to reduce inspiratory time and therefore reduce intrathoracic pressure and PVR -- to increase PBF. From CEACCP 2008 "The Fontan Circulation" - low respiratory rates, short inspiratory times, low PEEP and tidal volumes of 5-6ml/kg usually allow adequate pulmonary blood flow, normocarbia and low PVR ----------- |
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MC159 ANZCA Version [Apr 07]
The American Heart Association guidelines for pre-operative cardiac risk assessment define poor functional capacity as being only able to exercise at a level of less than 4 METS. An exercise capacity of 4 METS would correspond to: A. Light housework such as dishwashing B. heavy work around the house such as moving heavy objects C. jogging for 2 kms D. walking briskly on level ground (6kph) E. walking slowly on level ground (3kph) |
D. walking briskly on level ground (6kph)
6kph roughly equals 4mph. ACC/AHA Periop guidelines Table 3. 4 METS can be interpreted as either light housework or walking briskly. Suggest reading wiki ref. or Cleveland clinic JAN09 period assessment. ----------- |
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MC160 ANZCA Version [Jul 2007]
The strongest indication for the use of transoesophageal echocardiography during major non-cardiac surgery is A. recent myocardial infarction (less than six weeks old) B. acute significant intra-operative ST segment depression on ECG C. massive intraoperative blood loss D. a history of severe valvular heart disease E. unexplained significant intraoperative hypotension |
E. unexplained significant intraoperative hypotension
See ACC/AHA/ASE 2003 Clinical Application of Echocardiography Section XVI Intraoperative Echocardiography: Class I evidence: 1. Evaluation of acute, persistent, and life-threatening hemodynamic disturbances in which ventricular function and its determinants are uncertain and have not responded to treatment. ----------- |
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MC161 [Mar10][Aug10]
Drug eluting stent 6 months old. On aspirin and prasugrel 10mg. Elective lap cholecystectomy for biliary colic. A. Do case while taking both. B. Do case while stopping both. C. Stop Prasugrel for 7 days, keep taking aspirin. D. Stop Prasugrel for some other different time E. Post-pone for 6 months |
E. Post-pone for 6 months
Dual antiplt should continue for 365 days. Case is elective. Prasugrel is a new anti platelet drug similar to clopidogrel but with reduced MIs and rethrombosis but increased bleeding. Avoid in Pts <60kg or >75 or hx of TIAs and stroke (i think) see australian prescriber. ----------- |
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MC162 ANZCA version [Jul07][Apr08]
In acute coronary syndromes with ST elevation on ECG A. aspirin should be administered only after reperfusion strategies have commenced B. patients can wait up to 24 hours from onset of ischaemic symptoms before implementation of a reperfusion strategy C. patients should have elevated cardiac enzymes before proceeding to reperfusion strategies D. patients undergoing reperfusion strategies should have aspirin or clopidogrel but NOT both E. percutaneous coronary intervention is preferable to fibrinolytic therapy |
E. percutaneous coronary intervention is preferable to fibrinolytic therapy
See MJA 2006 April Suppl. S7 "In general, PCI is the treatment of choice, providing it can be performed promptly by a qualified interventional cardiologist in an appropriate facility." ----------- |
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TMP-Sep11-10
Patient indicated for prophylaxis of infective endocardititis A. amoxicillin orally 2 hours prior B. amoxicillin IV 1 hourly prior C. amoxicillin IV just before incision D. cefazolin IV 1 hour prior |
D. cefazolin IV 1 hour prior
From AHA 08 guidelines for dental procedure antibiotics should be given as a single dose 30-60min prior to procedure - Amoxicillin 2g po in adults or 50mg/kg in kids - Ampicillin 2g IV or IM or Cefazolin or Ceftriaxone 1g IM or IV if unable to take oral meds If allergic to penicillins or ampicillin - Cephalexin 2g po or - Clindamycin 600mg po (20mg/kg in kids) or - Azithromycin or clarithromycin 500mg (15mg/kg in kids) OR - Cefazolin 1g IV or IM or Clindamycin 600mg IM or IV ig unable to take oral meds. ----------- Prophylaxis against infective endocarditis is reasonable for pts at highest risk for adverse outcomes from infective endocarditis who undergo dental procedures that involve manipulation of gingival tissue or the periodical region of teeth or perforation of the oral mucosa: - pts with prosthetic cardiac valves or prosthetic material used for cardiac valve repair - pts with previous infective endocarditis - pts with CHD - unrepaired CHD, including palliative shunts and conduits - completely repaired CHD repaired with prosthetic material or device whether placed by surgery or by catheter intervention during the FIRST 6 MONTHS after the procedure. - repaired CHD with residual defects at the site of a prosthetic patch or prosthetic device (both of which inhibit endothelialization - cardiac transplant recipients with valve regurgitation due to a structurally abnormal valve |
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TMP-Jul10-010 [Mar11]
The best clinical indicator of SEVERE AS A. Presence of thrill B. Mean Gradient 30mmHg C. Area 1.2 cm2 D. Slow rising pulse and ESM radiating to carotids E. Shortness of breath |
A. Presence of thrill
see wiki. Dyspnoea may or may not be present in severe AS (though 50% of patients with severe AS will have dyspnoea). From "Aortic Stenosis and Non Cardiac Surgery" CEACCP 2005; 5(1):1-4 A - True - "A precordial thrill may be felt, especially on leaning forward in expiration. Its presence is reasonably specific for severe aortic stenosis" B - False - Severe AS mean gradient 40-50mmHg C - False - Severe AS valve area 0.6-0.8cm2 D - ? False - may be present in other grades of AS E - False - "There are three cardinal symptoms in aortic stenosis; angina, syncope and dyspnoea. However, symptoms do not correlate well to the severity of the stenosis" ----------- |
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TMP-Jul10-011
Elderly patient. Indications for pre Femoro-Popliteal Bypass angiogram include all EXCEPT: A. Severe heart failure B. Suspicion of L main disease C. Symptomatic tachyarrhythmia D. Unstable angina E. Stable angina with positive thallium |
C. Symptomatic tachyarrhythmia
- ?????? Much debate on wiki A. From UTD 'Overview of the therapy of heart failure due to systolic dysfunction': Myocardial revascularization with angioplasty or bypass surgery MAY improve symptom status, exercise capacity, and prognosis in selected patients with dysfunctional yet viable (hibernating or stunned) myocardium. Revascularization should also be considered in patients with a history of repeated episodes of acute LV dysfunction and flash pulmonary edema. B. Definite indication C. Would a pre-op angio change management? If they become tachycardic wouldn't you treat the arrhythmia anyway? D. Definite indication E. Depends on amount of myocardium at risk. From UTD 'Medical therapy vs revascularization in the management of stable angina pectoris': Radionuclide myocardial perfusion imaging can also be used to determine which patients with stable angina are more likely to have a survival benefit from revasculraization as opposed to medical therapy. The potential predictive value of rMPI was illustrated in a retrospective evaluation of more than 10000 consecutive patients without prior MI or revascularization who underwent exercise or adenosine rMPI. Of these, 671 underwent revascularization within 60 days after rMPI; the remainder was treated medically. At two years, mortality was significantly lower with revascularization in patients with inducible schema of >10% of total myocardium (2.6 vs 5.4 %). In contrast, mortality was significantly lower with medical therapy in patients with inducible schema of <10% of total myocardium (0.9 vs 3.3 %) ----------- |
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TMP-Jul10-022
A 4 year old child with VSD (repaired when 2 years old) for dental surgery. What antibiotic prophylaxis do the guidelines recommend? A. Amoxycillyn orally B. Amoxycillin IV C. Cephazolin IV D. Amoxycillin / gentamicin E. No antibiotics required |
E. No antibiotics required
According to the ACC/AHA 2008 Guideline Update on Valvular Heart Disease: Focused Update on Infective Endocarditis, routine antibiotic prophylaxis is no longer indicated for this patient. The patient had congenital heart disease, but it was repaired more than 6 months previously, and we are not told that there is a residual defect at (or adjacent to) the operative site repaired with prosthetic material which may impair/prevent endothelialisation. If this was the case, then prophylactic antibiotics would be indicated. ----------- |
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TMP-Jul10-056
[Mar11][Aug12] Thallium scan: A. High negative predictive value B. High positive predictive value C. Not as good as a dobutamine stress echocardiography D. E. |
A. High negative predictive value
- Thallium scanning in coronary artery disease (CAD) using radioactive thallium-201(201-Tl) is a widely available technique which is sensitive, accurate and noninvasive. It detects CAD accurately in patients with: atypical chest pain and a positive exercise ECG or typical chest pain and a negative exercise ECG. In known CAD, it determines the severity, extent and haemodynamic significance of a stenosis. In patients with recurrent chest pain following coronary artery graft surgery (CAGS) or angioplasty, scanning can detect the presence and severity of any ischaemia, when graft occlusion or restenosis has occurred. 201-Tl has important prognostic value in predicting cardiac complications (death and acute myocardial infarction) in patients undergoing major surgery - usually vascular. In patients with acute myocardial infarction, it may contribute to risk stratification. -from Aust Prescr 1994;17:57-61 Possibly 'A' depending on the stem. In the recent vascular surgery webinar/podcast Dr Machlin emphasised that, in the context of using perfusion scans to predict perioperative ischaemic events, a negative study was of much more benefit i.e. they have a high NPV but a low PPV. No one perfusion scan was any better than the others, it just depended what was available in your institution.SGB From the 2007 AHA guidelines, 'because of a very high sensitivity of abnormal stress nuclear imaging studies for detecting patients at risk for perioperative cardiac events, the negative predictive value of a normal scan has remained uniformly high at approximately 99% for MI or cardiac death' ----------- |
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TMP-Jul10-064 [Mar10]
[Sep11] Pregnant woman presents with narrow complex tachycardia HR 190, stable BP 100/60. No response to vagal manoevures. Management? A. Adenosine 6mg B. DCR C. Amiodarone D. Atenolol E. ? |
A. Adenosine 6mg
1. Acute Conversion of Atrioventricular Node–Dependent Tachycardias Intravenous adenosine is the drug of choice if vagal maneuvers fail to terminate an episode of PSVT. This drug has been used safely in pregnant women, although most of the reports of adenosine administration were in the second and third trimesters (202). If adenosine fails, then IV propranolol or metoprolol are recommended. Intravenous administration of verapamil may be associated with a greater risk of maternal hypotension and subsequent fetal hypoperfusion. Available data suggest that DC cardioversion is safe in all phases of pregnancy and can be used when necessary. ----------- |
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Version in March 2011:
Long stem about an old #NOF patient with aortic stenosis. What is a sign/ investigation/ symptom that shows the most severity? (ie Which one of these would indicate that the lesion was severe?) A: Thrill in Aortic area B: Murmur in lower left sternal edge C: Murmur radiating to carotids D: History of ischaemic heart disease or coronary artery disease E: history of angina/ syncope |
A
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Which is the best predictor of poor prognosis with aortic stenosis?
A. chest pain B. paroxysmal nocturnal dyspnoea C. syncope D. E. |
B
Syncope- 50% 3 year survival Angina- 50% 5year Dyspnoea- 50% 2 year ----------- |
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TMP-Sep11-056
[Mar12] You see a man in his 60s in clinic 1 week prior to laparoscopic cholecystectomy. He has dilated cardiomyopathy with an ejection fraction of 30%, but does not get dyspnoeic with normal activities of daily living. What is the most appropriate management of his heart failure? A. amiodarone 100mg bd B. digoxin 250mcg daily C. enalapril 2.5mg bd D. metoprolol 100mg bd E. diltiazem slow release 240mg daily |
C. Enalapril 2.5mg BD
See AHA 2007 CVS evaluation for non cardiac surgery AND AHA 2009 update for treatment of heart failure. Dose of metoprolol is extremely high to start with but he should also be started on a beta blocker. ----------- |
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MC135 [Jul06] Q122 ANZCA Version [Sep11]
You are called to the cardiac catheter lab to assist when a 55-year-old man with unstable angina becomes restless during difficult placement of a right coronary artery stent. When you arrive he is conscious and responding to voice. He is sweating with a pulse of 60 beats per minute in sinus rhythm, blood pressure measured from arterial catheter of 80/50 mmHg and Sp02 of 97%. The arterial pressure wave has an exaggerated fall with inspiration. The most appropriate next clinical intervention would be to A. administer atropine B. commence an adrenalin infusion C. perform a quick transthoracic echocardiograph D. sedate and intubate E. transfer to operating theatre immediately |
C. perform a quick transthoracic echocardiograph
(NB this is the ANZCA VERSION - black bank version mentions CVP of 2. Here (ANZCA version) they imply pulses paradoxus. It is likely he has tamponade but need a diagnosis before taking him to OT!) see wiki debate. ----------- |
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MC77 [Jul97] [Aug10][Sep11][?Aug12]
Which of the following does not cause diastolic dysfunction (type A) A. Hypertension B. Ischaemic heart disease C. Aortic stenosis D. Adrenaline E. Myocardial fibrosis (see also MC108) |
D. Adrenaline
The major causes of diastolic dysfunction include: • chronic hypertension • hypertrophic cardiomyopathy • aortic stenosis • coronary artery disease • restrictive cardiomyopathy (a rare condition in which the heart muscle is infiltrated, and made stiff, by abnormal cells, protein, or scar tissue. The most common cause of restrictive cardiomyopathy is amyloidosis, a disease in which protein-like substance is deposited within the body's tissues. Other causes include sarcoidosis and hemochromatosis.) • aging (Whether age alone causes stiffening of the ventricles, or whether such stiffening is related to "subclinical hypertension" or some other definable medical condition, is not yet worked out.) ----------- |
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TMP-Sep11-103
Repeat but different options Pulmonary hypertension secondary of lung disease- true A. Alpha agonist can be used B. Isoflurane will decrease the pulmonary pressure significantly C. N2O D. Ketamine E. Spontaneous breathing |
A
- ?need more info regarding question.. E has advantages and disadvantages. Aims of anaesthesia: - maintain adequate preload, SVT and contractility to allow RV to maintain CO - prevent increases in PVR from hypoxia, hypercarbia, acidosis, agitation, pain and hypothermia - hypotension should be aggressively treated with systemic vasoconstrictors such as phenylephrine (alpha agonist) or vasopressin to avoid decreased RV coronary perfusion and loss of contribution of IV septum to RV ejection. In patients with pulmonary hypertension, the most dangerous perioperative complication is systemic hypo- tension due to RV failure from exacerbation of pulmonary hypertension [49]. Although combined inovasodilators such as dobutamine and milrinone can be effective in increasing cardiac output in patients with pulmonary hypertension, owing to their systemic vasodilating effects they will not improve and may even exacerbate systemic hypotension. Systemic hypotension due to RV failure from pulmonary hypertension should be treated with inhaled vasodilators such as inhaled nitric oxide or inhaled iloprost. PDE-5 inhibitors may be useful preoperatively in preventing exacerbation of pulmonary hypertension or postoperatively in allowing weaning from inhaled pulmonary vasodilators [54]. ----------- |
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(Q132 Aug08) DC cardioversion - LEAST likely indicated for
A atrial fibrillation B atrial flutter C multifocal atrial tachycardia D paroxysmal atrial tachycardia E ventricular tachycardia |
C multifocal atrial tachycardia
- UTD (my summary) Multifocal atrial tachycardia is an arrhythmia that can be seen in a variety of clinical disorders. In addition to a heart rate greater than 100bpm, the characteristic eCG feature is variability in p-wave morphology, with each unique P-wave indicating a different site of atrial origin. It is associated with significant lung disease in 60% of cases. It can occur in presence of coronary, valvular, hypertensive and other types of heart disease, particularly when associated with heart failure and/or underlying lung disease. Affected patients tend to have which PCWP and pulmonary end diastolic pressures as well as a low-normal cardiac index. It is also associated with other disorders - hypokalaemia, hypomagnesemia, drugs (isoproterenol, aminophylline and theophylline), CRF. DC cardioversion is not effective. Other references indicate it may precipitate more dangerous arrhythmias. ----------- |
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TMP-Mar12-047
Features of ventricular tachycardia DO NOT include a. Absence of p waves b. Monophasic waves c. Prominent R wave in V1 d. A-V dissociation |
a. Absence of p waves - is NOT a feature of VT hence answer.
-- b. monophasic waves DO occur in VT - Monomorphic VT - regular rhythm, originates from a single focus within ventricles, produces uniform QRS complexes within each lead - each QRS is identical (except for fusion/capture beats) c. Prominent R wave in V1 - with a positive R wave in V1, three patterns are indicative of VT: smooth mono phasic Rwave, notched downslope to the R wave - the taller left rabbit ear (Marriott's sign), a qR complex (small Q, tall R) in V1. In contrast, RSR' pattern is suggestive of SVT with RBBB. d. A-V dissociation - this is seen in VT. - good reference: lifeinthefastlane.com ----------- |
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[Mar12] NEW: A lady with a Fontan’s circulation for tricuspid atresia presents for caesarian section. What is the best way of maintaining her cardiac output?
a. Trendelenburg b. Epidural contraindicated c. Allow pCO2 to rise to 50 to vasodilate her d. Short inspiratory time e. Allow hypovolaemia |
This is a remembered question. Answer may depend on exact wording.
maybe a. Tredelenburg or d. Short inspiratory time -- a. Trendelenburg - ?true; from J Clin Anaesth (2006) 18, 631-634 - Ideally, hypotension in the parturient after a Fontan correction should be treated with Trendelenburg/anti-Trendelenburg positioning and judicious use of fluids. Pharmacologic treatment may be problematic. b. false - Epidural is INDICATED; slow titration of epidural is better than spinal c. false - aim is to avoid increases in PVR, hypercarbia would worsen PVR d. Short inspiratory time - true… if she was under a GA e. false - important to maintain normovolaemia - need to avoid reduced preload ----------- |
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[Mar12][Aug12] You see a man in his 60s in clinic 1 week prior to laparoscopic cholecystectomy. He has dilated cardiomyopathy with an ejection fraction of 30%, but does not get dyspnoeic with normal activities of daily living. What is the most appropriate management of his heart failure?
See also TMP-Sep11-056 but different options. a. Frusemide b. Amiodarone c. ACE (I presume ACE inhibitor…) d. Digoxin e. Biventricular pacemaker f. stop beta blocker (option in Aug12) |
c. ACEI
-- a. Frusemide - false; indicated if he had stage B failure which is past or current symptoms of HF b. Amiodarone - false; should be avoided where possible. "Amiodarone should not be considered as part of the routine treatment of patients with HF, with or without frequent PVCs or asymp non sustained VT; HOWEVER it remains the agent most likely to be safe and effective when anti arrhythmic tx is needed to prevent recurrent AF or symptomatic ventricular arrhythmias" (2009 HF guidelines) d. Digoxin - false; Class III recommendation for stage B HF (i.e. nor recommended at all). See section in guidelines re: digoxin (essentially can improve symptoms but not primary Tx with acute exacerbation) e. Biventricular pacemaker - false; not first line tx. class IIa or IIb recommendation. -- NYHA I (no limitation in ordinary physical activity) and Stage B (structural heart disease but without signs or symptoms of HF). ACC AHA guidelines on heart failure 4.2 Class I recommendations - Beta blockers and ACEI should be used in all patients with a recent or remote history of MI regardless of EF or presence of HF - Beta blockers (level C evidence) are ACEI (level A) should be used in all patients with a reduced LVEF with no symptoms of HF even if they have not had an MI - ARB should be started to post-MI patients without HF who are intolerant of ACEI and have a low EF - Patients who have not developed HF symptoms: -- should be treated according to contemporary guidelines post acute MI; -- coronary revascularization is recommend in appropriate patients as per guidelines (in Mx of chronic stable angina) -- valve replacement or repair as per guidelines If he has had prior symptoms of HF it is Stage C heart failure in which case Frusemide is also indicated ----------- |
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[Mar12]
Wolf Parkinson White Syndrome: a. PR interval lengthened b. [Something about delta wave] c. DCR is less effective d. Central IV access may precipitate arrhythmias (see also MC114) |
d. Central IV access may precipitate arrhythmias
-- a. false - PR interval is short b. delta wave is due to accessory pathway from atria to ventricle (early depolarization of ventricle from a pathway other than AV node) c. false - DCR is effective d. true? ----------- |
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[Mar12] - new
[Aug12] Endocarditis prophylaxis A Bicuspid valve B Congenital repair > 12 months ago C Rheumatic heart valve D Uncorrected cyanotic heart disease E MVP + ?MR |
D. Uncorrected cyanotic heart disease
-- AHA ACC 2008 Guideline Update on Valvular Heart Disease: Focused Update on Infective Endocarditis Table 2 Class IIa 1. Prophylaxis against infective endocarditis is reasonable for the following patients at highest risk for adverse outcomes from infective endocarditis who undergo dental procedures that involve manipulation of either gingival tissue or the apical region of teeth or perforation of the oral mucosa: - Patients with prosthetic cardiac valves or prosthetic material used for valve repair - Patients with previous infective endocarditis - Patients with CHD -- Unrepairted cyanotic CHD, including palliative shunts or conduits -- completely repaired congenital heart defect repaired with prosthetic material or device whether placed by surgery or catheter intervention, drive first 6 months after procedure -- Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (both of which inhibit endotheliazation) - Cardiac transplant recipients with valve regurgitation due to a structurally abnormal valve ----------- |
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New: At what valve area do you begin to get symptoms, at rest, with mitral stenosis?
A. 1.5 cm2 |
A. 1.5 cm2
-- From "Modern Management of Mitral Stenosis" Circulation July 2005 Table 1 Moderate MS with MVA 1.2-1.6 cm2; Gradient 4-9 mmHg; Normal PAP; Class II symptoms. ----------- |
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TMP-131 [Oct09] [Aug10] [Sep11] [Aug12] Duration of Troponin elevation post myocardial infarction (also asked as cTnI)
A. 12-24 hours B. 24-48 hours C. 2-5 days D. 5-14 days E. 2-4 weeks |
D. 5-14 days
-- After myocardial cell damage, unbound cytoplasmic troponin is released from cardiac myocytes. Both troponin I and T exhibit biphasic release kinetics. Release from the cytosolic pool gives increase to blood concen- trations rising 4 – 6 h after the onset of damage and peaking at 12 – 24 h after myocardial injury. Structural protein release leads to a second peak 2 – 4 days after injury. Continuing breakdown of myofibrillary-bound complex explains the prolonged elevation of both troponins for up to 10 days after infarction. ----------- |
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[Apr09][Oct09][Mar10][Sep11][Aug12]
Pulsus paradoxus is: A. Reduced BP on inspiration unlike normal (ie normally increased on insp) B. Reduced BP on inspiration exaggerated from normal C. Reduced BP on expiration unlike normal D. Reduced BP on expiration exaggerated from normal E. ? (also asked Pulsus paradoxes in constrictive pericarditis:) |
B. Reduced BP on inspiration exaggerated from normal
By definition greater than 10mmHg fall. ----------- |
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TMP-130 [Oct09][Aug12] Essential diagnostic criteria on ECG for LBBB
A. Loss of septal Q's in V5 and V6 B. RSR in V1 C. Large slurred S in V6 D. T-waves opposite to direction of QRS E. QRS duration minimum 0.2 s |
A. Loss of septal Q's in V5 and V6
- Diagnostic Criteria - QRS duration of 120 ms - Dominant S wave in V1 - Broad monophasic R wave in lateral leads (I, aVL, V5-V6) - Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still allowed in aVL) - Prolonged R wave peak time > 60ms in left precordial leads (V5-6) ----------- |
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[Mar12][Aug12] NEW: Blood flow across which of the following is used to estimate pulmonary artery pressures during echocardiography?
A. Tricuspid valve B. Pulmonary valve C. Mitral Valve |
A. Tricuspid valve
-- But need TR. see online textbook on TOE. ----------- |
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TMP-Sep11-009b
[Mar12][Aug12] Which is the best predictor of poor prognosis with aortic stenosis? A. chest pain B. paroxysmal nocturnal dyspnoea C. syncope D. palpitations E. fatigue |
B. paroxysmal nocturnal dyspnoea
Patients die within an average of 5 yrs after onset of angina, 3 yrs after onset of syncope and 2 years after onset of heart failure symptoms. ----------- |
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TMP-Mar12-045 [Aug12]
A patient in recovery post op total hip replacement develops crushing central chest pain, ECG shows ST segment elevation (NB- no BP etc given, beta blockade was not an option). The most appropriate action is to give a. Aspirin b. IV GTN c. IV heparin d. Calcium channel blocker e. T/L |
a. Aspirin
or ??d. Calcium channel blocker -- a. With regards to aspirin, STRATAGEM trial found no difference with regards to thrombotic events or bleeding in patients who continued aspirin preoperatively for non cardiac surgery compared to patients who CEASED preop (though study is underpowered). Not sure how one can extrapolate these findings. PEP trial found trend toward a HIGHER risk of FATAL and non fatal MI in patients given periop aspirin… d. with regards to Ca channel blocker. From Perioperative Myocardial Infarction published in Circulation 2009 - "None of the randomized trials has shown reduced PMI or death, despite less supraventricular arrhythmia and ischemia in thoracic surgery. A meta-analysis of 11 trials found reduced combined perioperative death or PMI by posthoc analysis but more hypotension with calcium channel blockers." ----------- |
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TMP-Jul10-021 A 60 year old man describes orthopnoea. On examination: pansystolic murmur (at LSE)/ displaced apex beat. Likely diagnosis ?
A. Mitral regurgitation B. ? C. D. E. |
A. Mitral regurgitation
- VSD can also have pan systolic murmur but there will be other signs - also age of patient doesn't fit. ----------- |
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TMP-Jul10-041
New onset atrial fibrillation in a 10 week pregnant lady. BP 150/90, HR 160, SaO2 92%. Moderate mitral stenosis on TTE, no thrombus seen. Emergency doctor gave her anticoagulant (not specified what). Most appropriate management: A. Verapamil B. Labetalol 20mg iv to 300mg C. Amiodarone 300mg IV D. Synchronised biphasic cardioversion with 70-100 Joule E. Oral digoxin -1000mcg then 500mcg 6 hrs later |
D. Synchronised biphasic cardioversion with 70-100 Joule
- See wiki debate. From UTD Pregnancy in women with mitral stenosis: 'Sustained or frequent palpitations should be promptly investigated. Atrial fibrillation and other supraventricular tachycardia should be treated to prevent deleterious effect on uteroplacental perfusion. The key considerations in treating atrial fibrillation in pregnant women with mitral stenosis are prompt initiation of anticoagulation and rhythm control to prevent thromboembolic episodes and the risk of pulmonary edema. Low molecular weight heparin, or intravenous unfractionated heparin for hospitalized patients, is often used during pregnancy to avoid the potential teratogenicity and fetopathic effects of warfarin. Rate control with beta blockers or digoxin is the initial strategy for sustained atrial fibrillation. Beta blockers are more effective at heart rate control than digoxin as the renal clearance of digoxin is increased during pregnancy. As an elevated heart rate is crucial to maintain the augmented cardiac output in later pregnancy, the goal of ventricular rate control should be at 70 to 90 bpm rather than <60 bpm as in nonpregnant state. Electrical cardioversion should be considered when the ventricular rate or symptoms are responding poorly to rate control or when there is hemodynamic instability. If possible, transesophageal echocardiography should be performed prior to electrical cardioversion to exclude left atrial thrombus, which would be a contraindication to electrical cardioversion. The fetal safety profile will need to be considered when choosing an antiarrhythmic agent for maintenance of sinus rhythm.' Though patient is currently haemodynamically stable - her SpO2 are low and the concern is that she maybe developing pulmonary edema. ----------- |
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TMP-106 [Mar10][Aug10]
A 75yo male with moderate aortic stenosis (valve area 1.1cm2).. Gets mild dyspnoea on exertion but otherwise asymptomatic. Needs hip replacement. A. Continue with surgery B. Beta block then continue C. Get myocardial perfusion scan D. Postpone surgery awaiting AVR E. Postpone surgery awaiting balloon valvotomy |
C. Get myocardial perfusion scan (prev grp answer)
exclude ischaemia as cause for dyspnoea - much debate on wiki. A. ?possibility B. beta block then continue - false, unless there is any other indication for beta blockade C. ?true - from UTD 'Noncardiac surgery in patients with aortic stenosis': 'We suggest coronary artery disease assessment in asymptomatic patients with >2 risk factors for CAD who require INTERMEDIATE OR HIGH RISK SURGERY, given the high prevalence of concomitant disease in patients with AS. The following considerations guide the choice of test in patients with AS undergoing evaluation of CAD: - ECG stress testing is GENERALLY NOT SUFFICIENT for evaluation of CAD in pts with AS. Resting and exercise ECG in pts with valvular disease frequently show ST-segment changes due to LVH, LV dilatation or bundle branch block which reduces the accuracy of the test. - NON INVASIVE IMAGING (e.g. RADIONUCLIDE or echo) stress testing can be useful in patients with mild or MODERATE AS without baseline wall motion abnormalities. - Given the importance of determining the presence of CAD, angio remains most appropriate method for the definitive diagnosis of CAD in patients with severe AS. Non invasive imaging may not be helpful in patients with severe AS with LVH and/or chamber dilatation since resting or stress-induced regional wall motion abnormalities or myocardial perfusion abnormalities are nonspecific markers for CAD in such patients. Intermediate risk surgery (cardiac risk 1-5%) = intraperitoneal and intrathoracic surgery, carotid enarterectomy, head and neck surgery, ORTHOPAEDIC surgery, prostate surgery D and E - false. ----------- |
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TMP-109 [Mar10][Aug10]
The MAIN indication for biventricular pacing is A. complete heart block B. congestive cardiac failure C. VF D. E. |
B. congestive cardiac failure
cardiac resynchronisation Rx- dilated cardiomypathy, LVEF <35%, QRS>120 and NYHA III or IV despite maximal medical therapy - Indications are severe CM (EF<35%), LBBB with NYHA Class III or IV ----------- |
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TMP-128 [Aug09][Mar10][Aug10]
Indication for percutaneous closure of ASD A. Ostium primum < 3cm B. Ostium primum > 3cm C. Ostium secundum < 3 cm D. Ostium secundum > 3cm E. Sinus venosus ASD |
C. Ostium secundum < 3 cm
if large or complex or with an incomplete rim, referral for surgical closure is indicated. See CEACCP 2008 article 'Anesthesia for percutaneous closure of ASD' ----------- |
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TMP-112 [Mar10]
(similar to above) Patient for fempop bypass (i believe it said "angioplasty"), history of CCF. Also has diabetes on oral hypoglycaemics, controlled hypertension and atrial fibrillation at rate of 80bpm . A. Medium risk surgery, medium risk patient B. Medium risk surgery, high risk patient C. High risk surgery low risk patient D. High risk surgery, medium risk patient E. High risk surgery, high risk patient. |
D. High risk surgery, medium risk patient
- ACC/AHA guideline summary (Cardiac risk stratification for non-cardiac surgery) HIGH RISK (>5% risk of cardiac death or nonfatal MI) - Aortic and other major vascular surgery - Peripheral artery surgery INTERMEDIATE RISK (1-5% risk) - Carotid endarterectomy - Head and neck surgery - Intraperitoneal and intrathoracic surgery - Orthopaedic surgery - Prostate surgery LOW RISK (<1% risk) - Ambulatory surgery - Endoscopic procedures - Superficial procedure - Cataract surgery - Breast surgery Clinical predictors of increased period CVS risk MAJOR PREDICTORS that require intensive management and may lead to delay in or cancellation of the operative procedure unless emergent: - UA or severe angine or récent MI - Decompensated heart failure including NYHA IV or worsening or new onset HF - Significant arrhythmias including -- high grade AV block -- symptomatic ventricular arrhythmias -- supra ventricular arrhythmias with ventricular rate >100bpm at rest -- symptomatic bradycardia -- new VT Other clinical predictors that warrant careful assessment of current status - Hx of IHD - Hx of cerebrovascular disease - Hx of compensated heart failure or prior heart failure - DM - Renal insufficiency ----------- |
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TMP-Mar10-050
POISE trial showed A. Increase CVA B. Anaphylaxis C. renal failure D. Increased AMI |
A. Increase CVA
- POISE - PeriOperative Ischemia Study Evaluation. 8351 enrolled patients form 190 hospitals in 23 countries. 4174 pts received study drug, metoprolol succinate extended release (200mg daily, but down-titrated for hypotension or bradycardia to 100mg OD). The drug or placebo was started 2-4 h before surgery and continued for 30 days. Primary outcomes included total mortality, stroke, MI, coronary revascularization, AF, CHF, hypotension and brady cardia. The POISE results suggest that for every 1000 patients with similar risk profile undergoing non-cardiac surgery, metoprolol will prevent - 15 patients from suffering an MI - 3 patients from undergoing coronary revascularization - 7 patients from developing new significant AF HOWEVER will cause an EXCESS of - 8 patients to die - 5 to suffer a stroke (per 1000 treated) ----------- |
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++TMP-Mar10-081
Patient with diastolic dysfunction. Is it caused by: a. Restrictive cardiomyopathy b. Dilated cardiomyopathy c. d. e. |
a. Restrictive cardiomyopathy
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MN40 [Jul07][Apr08][Oct09][Mar10]
Correct statements regarding the autonomic nervous system include each of the following EXCEPT A. autonomic dysfunction is a predictor for worse long term survival after myocardial infarction B. heart rate responses are primarily mediated through the sympathetic nervous system C. inhalation anaesthetics all impair autonomic reflex responses D. autonomic dysfunction is a predictor for haemodynamic instability following anaesthetic induction E. low heart rate variability is associated with worse cardiac outcomes following non-cardiac surgery |
B. heart rate responses are primarily mediated through the sympathetic nervous system
Anesthesiology: Volume 90(3) March 1999 pp 651-653 - There also is strong evidence in patients that autonomic balance and vagal reflexes influence morbidity and mortality after MI. Patients surviving MI who had either low HRV or low baroreflex sensitivity had an increased risk of subsequent sudden cardiac death - The sympathetic component is primarily involved in adjusting peripheral vascular tone and plays a lesser role in the reflex regulation of HR and cardiac output. The vagal component is primarily involved in regulating HR. - it is well documented that patients with impaired autonomic reflexes (e.g., patients with diabetes) have greater intraoperative BP lability compared with autonomically intact patients. [2,3] In addition, it now is clear that many of the sedative, hypnotic drugs used for induction of anesthesia and all of the potent inhaled anesthetic gases in clinical use impair autonomic reflex responses. - low HR variability (HRV), an index of impaired cardiac-vagal tone, is an independent predictor of mortality after non-cardiac surgery ----------- |
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TMP-Oct09-038
ECG given. P pulmonale, Tall R V1, T inversion V1-3 a. Primary pulmonary hypertension. b. post. Infarct |
A. Primary pulmonary hypertension.
RVH= RAD, P pulmonale, T inversion V1-2 ----------- |
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[May09][Oct09]
60 year old vascular patient. ECG given. Showed large positive R waves in lateral leads, large negative S waves in anterior leads. ST depression laterally ie LVH with strain; bicuspid p waves A. LVH with strain B. Enlarged RA C. Lateral ischaemia D. LBBB E. L posterior hemiblock |
A. LVH with strain
- S waves in V1 or V2 and R waves in V5 or V6 added up to 35mm. ----------- |
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++TMP-Oct09-066
70 y old patient with AF (rate 80/min) in pre-admission clinic booked for ant resection. (it was not mentioned if AF was old or new or if on patient was on any medication) What management? A. Crack on B. Echocardiography and Cardioversion C. Immediate Cardioversion D. ? E. ? |
A. Crack on
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[May09] 2 month old systolic murmur heard at apex no change with posture, now on 5th centile for weight after being on 30th at birth, mother states has difficulty feeding. Peripheral pulses reduced femoral more than upper body. Most likely cause:
A. HOCM B. VSD C. PDA D. venous hum E. ASD |
C. PDA
- Asked again in Mar12 paper - but had coarctation listed as an option. Could not find anything related to weaker femoral pulses and above conditions. From wiki May09 page: PDA - collapsing pulse with sharp upstroke from ejection of large volume of blood into empty aorta during systole, low diastolic pressure due to rapid decompression of aorta, hyperkinetic apex, single S2 if large or even reversed splitting of S2, continous loud "machinary murmur at 1st LIC space. sometimes associated with flow murmur through left heart eg. mitral mid diastolic murmur. (Talley + O'Connor 3rd Ed.) If the pulmonary-to-systemic blood ratio approaches or exceeds 2:1, an apical flow rumble, caused by high flow into the left ventricle, is frequently present. Also, because flow through the left ventricle into the aorta is increased, an aortic ejection murmur may be present. History of difficulty feeding, low birth wt or poor growth, prematurity. www.emedicine.medscape.com ----------- |
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[Mar12] NEW Young infant with Failure to Thrive. Born on the 20th percentile now is on the 5th percentile. Found to have a systolic murmur, tachynpnea with weak femoral pulse. The most likely diagnosis is
a. Coarctation b. HOCM c. PDA d. AS |
a. Coarctation
- nb May 09 version did not have Coarctation in remembered version. ----------- |
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[Oct08] Post bypass 3 vessel CABG. Hypotensive and ECG shows ST elevation in II, aVF CVP 15mmHg PAP 25mmHg with normal SVR and PVR. What is most likely to be seen on TOE
a. early diastolic augmented flow ct atrial systolic flow b. Inferior hypokinesis (of the left ventricle) c. RV failure and TR d. Empty left ventricle following systole e. Mitral regurgitation |
c. RV failure and TR
OR b. Inferior hypokinesis (of the left ventricle) C>B - Inferior hypokinesis explains the ECG findings. Raised CVP and if PAP is mean then it is high (normal mean PAP 8-18) and is explained by RV failure and TR. ----------- |
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MC103 [Apr08][Oct08]
A 65 -year-old female patient with known chronic renal disease and a normal resting preoperative electrocardiogram (ECG) has undergone total hip replacement. Three days postoperatively she complains of chest pain and breathlessness. Her pulse rate is 110 min-1 and blood pressure 130/90 mmHg. The following ECG is recorded (((From remembered version it showed RBBB, R wave in VI, S wave in I, Q wave in III, t wave inversion in III (i.e. S1Q3T3). (Also had widespread ST elevation))) The diagnosis is most likely to be: A. Atrial fibrillation B. hyperkalaemia C. myocardial infarction D. pericarditis E. pulmonary embolus |
E. pulmonary embolus
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MZ79 [Jul07][Apr08]
[Sep11] In Marfan's Syndrome which is NOT related: A. If develop aortic disease most likely to be aortic stenosis B. At risk illiac aneurysm C. development of mitral valve prolapse is more likely than in general population D. Cardiac myopathy due to medial cystic necrosis/atrophy/ degeneration E. Intracranial aneurysm |
A. If develop aortic disease most likely to be aortic stenosis
False and answer to choose. More likely to get aortic REGURG due to aortic root dilatation. Marfan's syndrome ---------------- Characteristics: Inherited disorder of connective tissue metabolism. Tall with long/thin fingers, easy joint dislocation, high arched palate, emphysema, pectus excavatum, cataracts and retinal detachment, spontaneous pneumothorax, coronary thrombosis, dissecting aneurysms, aortic/mitral regurgitation, kyphoscoliosis. Key points: Associated abnormalities, minimize laryngoscopic response, control BP, central blocks acceptable. ----------- |
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[Apr 08] AZ
During which is procedure is it most important to reprogram a pacemaker? A. ECT B. MRI C. Lithotripsy D. Percutaneous transhepatic cholangiogram E. ? |
C. Lithotripsy
________________________________________ Anesthesia for Electroconvulsive Therapy A&A 2002; 94:1351-64 Patients with permanent pacemakers, a temporary conversion to fixed-rate pacing before ECT is recommended to minimize the risk of interference with pacemaker functioning as a result of inhibitory myopotentials. In patients with an automatic internal cardioverter defibrillator, the device should be deactivated before the electrical current is applied and should be reactivated in the early recovery period. ________________________________________ - MRI Contra-indicated in patients with pacemaker ________________________________________ Anaesthetic Management of Patients with Cardiac Pacemakers and Defibrillators for Noncardiac Surgery Annals of Cardiac Anaesthesia 2005; 8: 21-32 Lithotripsy Anaesthesia may be required in patients undergoing extracorporeal shock wave lithotripsy (ESWL) for immobilisation and to avoid pain in flank at entry site of waves. There may be electrical interference from hydraulic shock waves and can cause mechanical damage. High-energy vibrations produced by lithotripsy machine can cause closure of reed switch causing asynchronous pacing. ‘Activity’ rate responsive pacemaker can be affected due to the damage caused to the piezoelectric crystals by ESWL. The shock waves can produce ventricular extrasystoles, if not synchronized with R wave.9 Thus, pacemaker malfunction can occur in patients undergoing ESWL, requiring adequate preparation prior to procedure. One should have cardiologist’s opinion, perioperative ECG monitoring, device programmer and a standby cardiologist to deal with any device malfunction. Rate responsive pacemaker should have their activity mode deactivated. Focal point of the lithotriptor should be kept at least six inches (15 cm) away from the pacemaker.30,31 Patient with abdominally placed pacemaker generators should not be treated with ESWL. Low shock waves (<16 kilovolts) should be used initially followed by a gradual increase in the level of energy.32 Dual chamber demand pacemaker is especially sensitive to shock waves and should be reprogrammed to a simpler mode (VOO, VVI ) preoperatively. ________________________________________ Percutaneous transhepatic cholangiogram - can't see why ----------- |
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TMP-Oct09-018
Patient with known severe aortic regurgitation. Auscultation reveals loud mid diastrolic murmur in aortic area. You also hear a quiet mid diastolic murmur in the apex. This is a. Functional mitral stenosis b. Mitral valve incompetence c. Impaired LV function d. Papillary muscle dysfunction |
A. Functional mitral stenosis
Backflow from AR occludes flow from the atria causing a functional obstruction to flow across the MV = Austin-Flint Murmur ----------- |
