Toronto Internal Medicine Review 2024 PDF

Toronto IMR 2024 Slides good luck! MedStore Medical Supplies  BONUS E-LECTURE: Allergy & Clinical Immunology With Contributions by Dr. Andrea Burke and Dr. David Fahmy Clinical Immunology & Allergy Primary Immunodeficiency (PID) Ten Red Flags of Immunod...

Toronto IMR 2024 Slides good luck! MedStore Medical Supplies  BONUS E-LECTURE: Allergy & Clinical Immunology With Contributions by Dr. Andrea Burke and Dr. David Fahmy Clinical Immunology & Allergy Primary Immunodeficiency (PID) Ten Red Flags of Immunodeficiency: 1. ≥ 2 new ear infections within 1 year 2. ≥ 2 new sinus infections within 1 year, in the absence of allergy 3. One pneumonia per year for more than 1 year 4. Chronic diarrhea with weight loss 5. Recurrent viral infections (colds, herpes, warts, condyloma) 6. Recurrent need for IV antibiotics to clear infections 7. Recurrent, deep abscesses of the skin or internal organs 8. Persistent thrush or fungal infection on skin or elsewhere 9. Infection with normally harmless tuberculosis-like bacteria 10. A family history of Primary Immunodeficiency 2  Primary Immunodeficiency (PID) General Approach: Rule out secondary causes of immunodeficiency: – DM, HIV infection, Cirrhosis, Nephrotic syndrome, Autoimmune disease, Malignancy, Splenectomy/Asplenia, Immunomodulatory drugs – Structural (obstructive tumours, urethral strictures), dermatitis, burns Identify type of infections (see below) to direct investigation PREDOMINANT INFECTIONS TYPE OF IMMUNO- Investigations DEFICIENCY Repeated pyogenic infections B- cell Lymphocyte count, Lymphocyte subsets, Immunoglobulins (IgG, IgA, IgM), vaccination titres Severe mycotic infection and T- cell Lymphocyte count, Lymphocyte subsets opportunistic infections Abscess-forming infection with Neutrophil deficiency Neutrophil count, Chronic Granulomatous low-grade pathogens Disease (CGD) Assay Repeated infections w/ Complement C3, C4, CH50 Neisseria sp. deficiency  Immunodeficiency to know: CVID Combined Variable Immunodeficiency (CVID) Most common symptomatic PID in adults – Recurrent sinopulmonary infections – Dx: LOW IgG + LOW IgA or IgM + poor response to vaccination; other immunodeficiency causes ruled out (e.g. CLL) – Tx: IVIG or SCIG (sub-cutaneous Immunoglobulin) 4  Urticaria (1) Acute Urticaria Common antigens/triggers = antibiotics (PCN, Sulfa), NSAIDs, insects, food (shellfish in adults) - if there’s a trigger, there will be an obvious relationship Lasts < 6 weeks Work-up: Allergy referral for skin testing First line treatment: STOP medication/AVOID trigger if identified, anti- histamines PRN: ex. Cetirizine (Reactine) Red Flags of Urticaria: Typical Urticaria: Last longer than 48hr Last 6 weeks, most days of the week, “Spontaneous”: no clear trigger Workup of CSU – CBC + diff, ESR/CRP Workup of other causes of chronic urticaria – as directed by clinical picture: – Autoimmune work-up: ANA, ds-DNA, RF – Serum tryptase if systemic symptoms [Mastocytosis] – Biopsy [urticarial vasculitis] Treatment of CSU – 1st line: Daily non-sedating antihistamine (cetirizine) – 2nd line: increased dose non-sedating antihistamine (4x – 3rd line: Omalizumab (Xolair) Physical Chronic Urticaria Trigger = Pressure (aka dermatographism), Heat, Cold  Angioedema Angioedema + pruritus/urticaria = most likely Mast cell mediated Acute Treatment Angioedema: Related to a Specific Trigger (food, drug, insect bite, etc.) STOP offending agent/trigger, if possible Idiopathic Angioedema (can be part of CSU) H1-Blocker: Diphenhydramine 25-50mg IV H2-Blocker: Ranitidine 50mg IV Angioedema (NO pruritus/urticaria) = Mast cell OR Bradykinin-mediated Steroids: Methylprednisolone ~60-80mg IV Differential diagnosis: *Anaphylaxis or oropharyngeal angioedema: Epi! – Related to Specific Trigger (see above) ACE Inhibitor Angioedema: Icatibant – Idiopathic Angioedema Known HAE: skip above treatment, instead: C1 Chronic Tx: Frequent episodes : Daily antihistamine (Cetirizine) esterase inhibitor, Icatibant Rare episodes: Prednisone + antihistamine for first sign of symptoms Investigations: Epinephrine Auto-injector Type C1 Inhibitor C1 Inhibitor C4 Level Function – Hereditary Angioedema (HAE): C1 esterase inhibitor deficiency – Types I, II, III HAE Type I Low Low Low PEARL: in general, a normal C4 level (in acute setting) rules OUT HAE Type II Normal/High Low Low HAE Types I &II HAE Type III Normal Normal Normal Chronic Tx: Prophylactic C1 esterase Inhibitor Acquired Low Low Low – Acquired Angioedema (lymphoproliferative or autoimmune disease) ACE In Normal Normal Normal – ACE Inhibitor Angioedema Idiopathic Normal Normal Normal NEW: NEJM 2015: A Randomized Trial of Icatibant in ACE-Inhibitor–Induced Angioedema Conclusion: in this RCT involving patients with ACE-inhibitor–induced angioedema, complete resolution of edema was achieved significantly more quickly with SQ icatibant than with standard therapy consisting of glucocorticoids and antihistamines.  Anaphylaxis Common Triggers: food, medica2on, latex, insect venom Diagnosis: see next slide Acute Treatment IM EPINEPHRINE – ABCs, MOIF 0.01 mg/kg (max 0.5mg) IM Repeat q5-15 min PRN – STOP drug/REMOVE trigger (if iden2fied) Note: 1:1000 solution = 1mg/mL – Epinephrine IM: 1:1000 (1mg/mL) – DOSE: 0.01mg/kg (max 0.5mg) IM in anterolateral thigh, repeat q5-15min IV EPINEPHRINE 0.05-0.1 mg IV over 5 min – Epinephrine IV: 1:10,000 (0.1mg/mL) – BOLUS: 0.05-0.1 mg IV over 5 Then infuse 2-10 mcg/min titrated min, then INFUSE: 2-10mcg/mL to BP Consider IV aXer several (i.e. 3) doses IM, profound hypotension, obese Note: 1:10,000 solution = paZents 0.1mg/mL Adjunc2ve medica2ons: – H1-Blocker: Rani8dine 50mg IV q8hr PRN – H2-Blocker: Diphenhydramine 25-50mg IV q4-6hr PRN – Steroids: Methylprednisolone 125mg IV q6hr PRN Discharge Plan: Prescribe Epinephrine Autoinjector 0.3mg – Glucagon – paZents on beta-blockers IM PRN – Salbutamol – paZents with signs of bronchoconstricZon Anaphylaxis Action Plan – Vasopressors – for persisZng hypotension Patient/Caregiver Education Observe un2l symptoms improving, min. 4-6hr MedicAlert bracelet Referral to Allergist/Immunologist ANAPHYLAXIS: Clinical Criteria for diagnosis Kim & Fischer AACI 2011, 7(Suppl 1):S6 Anaphylaxis is highly likely when ANY ONE of the following 3 criteria is fulfilled following exposure to an allergen: 1. Acute onset of an illness (min to several hours) with q Skin or mucosal tissue involvement (or both) Generalized hives, itch/flushing, swelling of lips/tongue/uvula ANAPHYLAXIS = AND at least ONE of the following: one of: q Respiratory compromise 1. Possible Dyspnoea, wheeze, bronchospasm, stridor, reduced PEF, hypoxemia allergen + q Hypotension or associated symptoms of end-organ dysfunction Skin/mucosa Hypotonia, syncope, incontinence + ≥ 1 of Resp 2. TWO or more of the following that occur rapidly (min to several hours) after exposure to a likely allergen for HoTN/EOF that patient q Skin or mucosal tissue involvement 2. Likely Allergen + Generalized hives, itch/flushing, swelling of lips/tongue/uvula ≥ 2 of q Respiratory compromise Skin/mucosa Dyspnoea, wheeze, bronchospasm, stridor, reduced PEF, hypoxemia Resp HoTN/EOF q Hypotension or associated symptoms of end-organ dysfunction GI Hypotonia, syncope, incontinence q Persistent GI symptoms 3. Known Painful abdominal cramps, vomiting Allergen + 3. Hypotension after exposure to a known allergen for that patient (min to several hours) HoTN q Adults: sBP 30% decrease from patient’s baseline PEARL: As a general rule, any time you have more than one system involved, you should suspect anaphylaxis!  Penicillin Allergy Approach: – IgE-Mediated: pruritus, urticaria, angioedema, etc. – Non-IgE-Mediated: SJS-TENS (blistering, desquamation, conjunctivitis), DRESS (eosinophilia, fever, end-organ involvement), serum sickness (arthritis, fever) Management: IgE-mediated Reactions – Allergy referral for Penicillin Skin Testing + Oral Challenge ~90% “PCN allergic” patients will test negative – can safely receive beta-lactam and cephalosporin antibiotics Positive skin test – AVOID penicillin, higher likelihood of reacting to 1st gen cephalosporins – Drug Desensitization (under close observation, OK to do even in Pregnant patient (eg) with syphilis)) If penicillin is required acutely and no time for skin testing, or skin test positive Note: this is a temporary induction of ‘tolerance’, and does NOT rule out allergy Note: this is only used in cases of IgE-mediated drug reactions (NOT if any suspicion of serum sickness, SJS-TENS, DRESS, etc.) – Note: Aztreonam (monobactam) – generally tolerated in penicillin allergic patients exception: if they have reacted to ceftazidime! Patient history not very reliable (JAMA 2001): PCN allergy history positive: LR+ 1.9 for +ve skin test PCN allergy history negative: LR- 0.5 for +ve skin test  Example Question A 30-year-old woman presents with a second pneumonia in the last six months. She has a past medical history of recurrent pneumonias and sinusitis. Investigations show: WBC 6, Neutrophils 3, Lymphocytes 2, Monocytes 1. What is most likely diagnosis? 1. Complement deficiency 2. Common variable immunodeficiency 3. HIV 4. Chronic granulomatous disease  Answer A 30-year-old woman presents with a second pneumonia in the last six months. She has a past medical history of recurrent pneumonias and sinusitis. Investigations show: WBC 6, Neutrophils 3, Lymphocytes 2, Monocytes 1. What is most likely diagnosis? 1. Complement deficiency 2. Common variable immunodeficiency 3. HIV 4. Chronic granulomatous disease  Example QuesEon A middle-aged female presents with a 6 month history of urticaria. She has never had any episodes of swelling. The urticaria resolve within 12hr, with no residual bruising or scarring. She reports that she has been eating out at restaurants more recently. She is otherwise well. Initial bloodwork is normal including a CBC, creatinine and liver profile. What is the most likely cause of this patient’s symptoms? 1. Chronic Idiopathic Urticaria 2. Food allergy 3. C1 esterase deficiency 4. Autoimmune Disease  Answer A middle-aged female presents with a 6 month history of urticaria. She has never had any episodes of swelling. The urticaria resolve within 12hr, with no residual bruising or scarring. She reports that she has been eating out at restaurants more recently. She is otherwise well. Initial bloodwork is normal including a CBC, creatinine and liver profile. What is the most likely cause of this patient’s symptoms? 1. Chronic Idiopathic Urticaria 2. Food allergy 3. C1 esterase deficiency 4. Autoimmune Disease  Example Question A pregnant patient with a history of asthma states she is allergic to penicillin. She developed wheeze the last time she took it, while admitted for an upper respiratory tract infection. She was referred for penicillin skin testing, which was negative. Penicillin is now indicated for a pregnancy acquired syphilis infection. Which drug would you use? 1. Penicillin 2. Second-Generation Cephalosporin 3. Doxycycline  Answer A pregnant patient with a history of asthma states she is allergic to penicillin. She developed wheeze the last time she took it, while admitted for an upper respiratory tract infection. She was referred for penicillin skin testing, which was negative. Penicillin is now indicated for a pregnancy acquired syphilis infection. Which drug would you use? 1. Penicillin 2. Second-Generation Cephalosporin 3. Doxycycline  Example QuesEon A young man presents with occasional angioedema of his lips and hands. Which of the following features make it least consistent with C1 esterase deficiency? 1. Occasional GI symptoms 2. Triggered by dental procedure 3. Presence of urticaria 4. Laryngeal involvement  Answer A young man presents with occasional angioedema of his lips and hands. Which of the following features make it least consistent with C1 esterase deficiency? 1. Occasional GI symptoms 2. Triggered by dental procedure 3. Presence of urticaria 4. Laryngeal involvement Applied Scenarios & Ethics Primer ONLINE ONLY LECTURE NOTES © Internal Medicine Review 2024  Overview Types of Applied Scenarios – General Approach to Clinical Scenarios Ethics – Patient Centred Communication – Consent and Capacity – Fitness to Drive – Troubled Colleague / Professionalism – End of life care – Disclosure of medical error – Confidentiality Patient Safety/QI àSee Online PRIMER with examples Truth and Reconciliation in Canada – implications for physicians  Applied / Oral Scenarios In 2023, your applied / oral scenario will be done virtually. Unless you have a medical exemption for accommodation, you will have to do this at one of 17 hotel test centres in Canada – On a computer, with examiner virtually What we know about virtual Applied/Oral Exams (https://www.royalcollege.ca/rcsite/documents/ibd/internal-medicine-examformat-e) – 7 virtual stations x 18 min each 1 rest station , 6 “work” stations May have >1 case per station – (eg) read stem 1-2 min, then 7 min scenario, read next stem 1-2 min, 7 min scenario – Media provided can include videos [NB none reported in 2022] or documents (eg ECG – usually opens in a separate window) – Although the virtual format does not lend itself to physical exams, we have been told that knowledge of exam maneuvers may be tested (eg. – describe how to measure a pulsus paradoxus) 3 Feedback from IMR2023 Attendees “[Need to practice interruptions causing] stress that is experienced on exam day. I think that on the “ On the real exam there were board exam the examiners do not many doublet stations where we really give you time to go over all only had 1 min to read and were the management including non- pressured to have a differential and pharm treatment. You would get plan ready to go right away. ” interrupted to move onto the next question. ” “The real exam has become very rapid fire. Long stem with HPI, P/E and initial Ix then after the prep time it’s really just “what’s “There seems to be more of a your ddx and how would you manage, focus on providing differential, including further investigations?” They’d show you an EKG or X-ray if that was investigations, management and relevant to your workup. They cram so much answering specific questions in 7.5 into the stations … that you really can’t stray minutes.” from the relevant points of the case (in an attempt to pick up extra points for non- pharm things, for example) some of the examiners were quite abrupt.” 4  Types of Applied Scenarios Emergency Department / Ward on-call – (eg) Patient presenting after travel from Africa with fever and jaundice – workup and manage Pre- or Post-op patient – (eg) Elective Orthopedic patient seen preop, asked to manage meds, calculate RCRI, manage MINS postop Pregnant patient – (eG) L&D / ED – hypertension, pre-eclampsia diagnosis, admission, management Office Scenario – (eg) Patient with diabetes – BP, A1C, Lipids all above target “how would you optimize”? Prompts to cover counselling of patient – driving, eye exams, etc. Communication Station Unlikely – In 2022 & 2023 no role-playing was reported however website still states Applied exam designed to test CANMEDs roles (including communicator). You may be asked how you would counsel a patient on a procedure or treatment (Indications, Contraindications, Risks, Benefits, Risks if you don’t have intervention…) – Ethics come up - Know Canadian Laws around medicolegal issues of care: Driving, end of life,consent & Capacity, withdrawal of care, MAID  Clinical Scenarios: General Approach 1. Understand the question – If provided with a long stem, check the question at end first to tailor your reading – If your task is unclear from the written stem you are given, ask to clarify “Do you want me to counsel this patient on anticoagulation for atrial fibrillation only or other aspects of Afib management such as rate/rhythm control?” 2. Frame and Markup your “Pink Sheet” [you will be given a piece of paper to take notes on for each scenario] – Your Differential – do this every time, may get asked by examiner what DDx is – Management Tests for workup: many provided in stem if it is a management scenario Be prepared: ECG, CXR, PFTs are fair game for interpretation Non Pharm: SPEDD – Smoking, Pregnancy, Exercise, Driving, Diet Pharm: Acutely ill: ABC MOIF (monitor, oxygen, IV, foley) C&C (consults and code status) 3) Answer the Question – with new format, you will get pushed towards management 6  Clinical Scenarios: General Approach Management PEARLS: ACUTE MANAGEMENT Use common sense – in an ED scenario with unstable patient, you must treat first, investigate later (like in real life!) – (eg) Afib –BP 70/40, HR 160, patient stuporous “This patient is presenting with acute unstable SVT/AFIB – I would like to move to appropriate resus area of the ER and begin ACLS measures” – Cardiovert first, ask questions later – (eg) ECG may suggest WPW but if unstable just cardiovert then think about next steps! – (eg) ED Tox Scenario – patient starts to seize: Treat Seizure (position, suction available, oxygen, give appropriate order for benzodiazepine) “While the nurse is preparing the lorazepam I would ask for the following stat labs including an immediate capillary glucose and ECG…” – UNSURE? SAY WHO YOU WOULD CALL, WHAT YOU WOULD LOOK UP. (Like in real life.). This is a safety scenario – if you can demonstrate knowledge gap and where you would seek answer or help this is a PASS. 7  Clinical Scenarios – General Approach Management (continued) : SUBACUTE “C&C = Consult and Counsel” Consult appropriate services – “I would consult a hematologist and ICU where plasma exchange is available for this patient with TTP for transfer…” – Pregnant Scenario: Don’t forget to consult OB +/- anesthesia +/- Paeds Counsel – I would counsel the patient as to… Medicolegal: Driving? Work restrictions? Communicable disease / Public Health reporting requirement? Risk of recurrence? (ex. DVT or HTN in pregnant pt) Consequences of disease (ex. Afib à Stroke risk) Consequences of treatment (ex. Afib à anti-arrhythmic side effects), Pregnancy implications if childbearing age. 8  Ethics In exams before 2020, there was usually a role-playing communication station. Now with virtual format, it is more likely a question of ethics will come up in a management question. (eg) question of consent/capacity in a patient with Jehovah’s witness faith refusing blood, driving restrictions post ICD or stroke Patient Centred Communication – A Canadian Healthcare Priority Consent & Capacity Fitness to Drive Troubled Colleague / Professionalism End of life care – Medical Assistance in Dying (MAID) – Withdrawal of care Disclosure of adverse events / medical error – Patient Safety / Quality Improvement may be asked Confidentiality Patient Safety / QI  Patient Centred Communication Meeting a patient “where they are” and acknowledging the socioeconomic and cultural influences on health (social determinants of health (#sdoh)). FIFE –ask patients about their Feelings (fears) around illness, Ideas about what has caused illness, how it affects their Functioning, and Expectations of their encounter and treatment (eg) Creating a safe space for gender identity – inviting patients to express gender with preferred pronouns (eg) Being aware of non-visible aspects of culture – such as how emotions are managed, how modesty and physical distancing affect comfort with physical exam (eg) Writing “The patient is noncompliant with dietary recommendations for diabetes” does not acknowledge how food insecurity may make it impossible for patient to comply with your recommendations – screen for SDOH 10  Consent & Capacity Scenarios to consider: – The patient who is refusing life-saving therapy Diabetic refusing above knee amputation Jehovah’s Witness refusing transfusion – The family member who asks for a treatment for their cognitively impaired parent. Variation: Family member who does not want you to disclose terminal diagnosis to their parent  Consent Requirements 1. Voluntary 2. Informed 3. Capable 4. Documented in the Chart* (*my lawyer added this) CMPA Consent and Capacity Module https://www.cmpa- acpm.ca/serve/docs/ela/goodpracticesguide/pages/communication/Informed_Consent/informed_consent- e.html Assent ≠ Consent (just because a patient lets you do a procedure (ex. ABG) does not mean that you have their consent.)  Consent: Voluntary No compulsion – By physician – By other 3rd party Police officer Family member  Consent : Informed Informed consent components – “Reasonable Patient Standard” – Supreme Court What a reasonable patient in the particular patient's position would have expected to hear before consenting. – Description of treatment – “Material Risks” “A risk is thus material when a reasonable person in what the physician knows or should know to be the patient's position would be likely to attach significance to the risk or cluster of risks in determining whether or not to undergo the proposed therapy.” – Alternates to treatment (and risks of alternate) Informed by MD carrying out procedure – Can be delegated (ex. to a resident) if delegate has sufficient knowledge and experience to provide explanations  Consent : Capable patient An individual who is able to understand – the nature and anticipated effect of proposed medical treatment and alternatives – Understand and appreciate the consequences of refusing treatment (Source: CMPA Guide to Consent) Capacity may fluctuate in hospital Consent : INcapable patient If your patient is incapable – identify an appropriate substitute decision maker (SDM) – do not get fooled in a scenario! Ontario SDM Hierarchy: 1. Power of Attorney for Personal Care 2. Spouse, Common-law spouse* or Partner 3. Parent or adult (>16yrs) children 4. Siblings 5. Any other family member by blood, marriage or adoption 6. Public Guardian & Trustee If there is a CONFLICT between SDMs à PG&T should make decision in their stead (e.g. if SDMs are son and daughter who completely disagree on treatment)  *Common Law for Health Care Ontario: – have cohabited for at least one year – have a child together – have entered into a cohabitation agreement together. Quebec: – ?? Different sources quote different laws (0-3 years cohabitation) Alberta: – Have cohabited for three years B.C.: – Have cohabited for two years 17  Consent & Capacity Scenarios to consider: The patient who is refusing life-saving therapy – Diabetic refusing above knee amputation – Jehovah’s Witness refusing transfusion The family member who asks for an opinion/treatment for their cognitively impaired parent. – Variation: Family member who does not want you to disclose diagnosis of cancer to their parent. – Patient who does not want to hear details of diagnosis, “Doctor do what you think is best”  Consent & Capacity Scenarios to consider: – Patient who does not want to hear details of diagnosis, “Doctor do what you think is best” CASE LAW: You can treat a patient without them being fully informed if they waive their autonomy with respect to consent – make sure their decision to waive this is properly informed + capable of course! [Ontario Health Care and Consent Act doesn’t make a ‘ruling’ on this – it is OK to say in your scenario to patient that you will need to speak to ethicist/CMPA, that you respect their decision and wishes and just need to be sure what your medico-legal obligations are.] Fitness to Drive Available for free to CMA Members Also note CCS 2023 published new guidelines on fitness to drive after cardiac illness – these are reviewed in Cardiology Lecture @ IMR2024 and summaries below. 20  Fitness to Drive Consider: Truck Driver with visual field impairment New Seizure – counsel on driving Sleep Apnea – non compliant with CPAP  Fitness to Drive - CMA Duty to report – Varies province to province including duty to report Alberta, Nova Scotia, Quebec = reporting discretionary – In Ontario (Exam is in Ottawa so default to Ontario rules if unsure) – MDs must fill out medical condition report and cannot be legally challenged for doing so: “Medical Condition Report Ontario” – Ontario Ministry of Transportation suggests the CMA guide be used by physicians in determining requirements to report  CMA Fitness to Drive: https://joule.cma.ca/en/evidence/CMA-drivers-guide.html Category Private Car Commercial Driver (Truck, Bus) Cognitive Hepatic Encephalopathy No Driving Dementia UPDATED IN 2019 – SEE NEXT SLIDE Psychiatric – acute psychosis, lack of No driving coopertion w/ treatment or treatment too sedating Stroke Untreated intracerebral aneurysm No driving Postop Aneurysm Rx 3 mos 6 mos Other stroke, with normal VF, neuro 1 month 1 month exam Alcohol Alcohol Withdrawal Seizures Seizure free, alcohol free for 6 months – Dependence Rehabilitated and Compliant  CMA Fitness to Drive: https://joule.cma.ca/en/evidence/CMA-drivers-guide.html Category Private Car Commercial Driver (Truck, Bus) Sleep Problems OSA – mild or treated (TREATED = at Safe to Drive least 4 hrs/d, 70% of last 30 days) OSA – mod/severe untreated No driving Narcolepsy No driving Endocrinology Diabetes on insulin May drive if: medic alert worn, no severe hypoglycemia last 6 mos Seizure Single, unprovoked, no epilepsy 3 months EEG, imaging Full workup to ID required – if normal cause 12 mos Epilepsy compliant on medications 6 mos seizure 5 years seizure free free  CMA Fitness to Drive : Dementia Diagnosis of dementia alone not sufficient reason to suspend license. – Discuss a plan to “retire” from driving with patient – Physician is not the one to determine who is fit to drive, but to report clinical findings that raise concern about ability to drive Where fitness to drive not clear, refer for further functional testing (e.x. OT, DRIVEABLE assessment) Ask : would I let a loved one get in the car… would I want a loved one crossing street in front of this individual’s car...? If answers are uncertain or “NO” then report and refer for further testing. 25 CMA Fitness to Drive: Dementia Excerpts 26 CMA Fitness to Drive: Dementia Excerpts 27  CMA Fitness to Drive: https://joule.cma.ca/en/evidence/CMA-drivers-guide.html Category Private Car Commercial Driver (Truck, Bus) VISION Visual Acuity ≥20/50 Corrected ≥20/30 Corrected both both eyes open eyes open Visual Fields 120 continuous degrees 120 continuous degrees along horizontal along horizontal meridian meridian 20 continuous degrees 15 continuous degrees above and below fixation above and below fixation  CCS 2023 Fitness to Drive Guidelines Category Private Car Commercial Category Private Car Commercial Driver Driver (Truck, Bus) (Truck, Bus) STEMI/NSTEMI 2 weeks post d/c 1 months post NYHA I OK to drive LVEF ≧ 30% OK with LVEF >40% d/c NYHA II OK to drive LVEF ≧ 30% OK STEMI/NSTEMI 1 month post d/c 3 months post NYHA III OK to drive NO DRIVING with LVEF ≦ 40% d/c NYHA IV NO DRIVING NO DRIVING Coronary STEMI/NSTEMI 1 month post d/c 3 months post Home NO DRIVING NO DRIVING Artery with no PCI d/c Heart inotropes Disease* performed Failure** LVAD 2 months after NO DRIVING UA (ACS without 48h w/ PCI 7 d w/ PCI implant if NYHA 1-2 MI) 7 d w/o PCI 1 month w/o PCI Heart 6 weeks after 6 months post transplant discharge + NYHA 1-2 discharge + PCI in non-ACS 48h 48h + stable NYHA 1 + LVEF context immunosuppression + ≧ 50% + Asymptomatic OK to drive OK to drive followed annually followed CAD, stable angina annually CABG 1 month post d/c 3 months post d/c *Updates focus on LVEF post MI, regardless of mechanism **Updates provide new recommendations for LVAD/TxP  CCS 2023 Fitness to Drive Guidelines Category Private Car Commercial Driver (Truck, Bus) Medically treated AS: OK if NYHA 1-2 Only OK if in the lowest risk group: NYHA 1, no AS, AI, MS, MR, TR syncope, LVEF ≧ 50% MS, MR, AI, TR: OK if NYHA 1-3 AS, AI: as above MR: also no pHTN or systemic embolism MS: no LVEF requirement TR: no RV dysfunction, symptomatic RV failure, RV Valvular arrhythmias Heart Post TAVI or SAVR for AS, AR 1 month if stable QRS duration, no 3 month if stable QRS duration, no high grade AV Disease high grade AV block (2nd type II or block (2nd type II or 3rd) if no PPM and NYHA I 3rd) if no PPM and NYHA I-III AR requires as above + LVEF ≧ 50% AR requires as above + LVEF ≧ 50% Post TEER for MR or TR 48h post d/c if NYHA I-III 1 month post d/c if NYHA I and LVEF ≧ 50% Post balloon valvuloplasty for MS 48h post d/c if NYHA I-III 1 month post d/c if NYHA I Post TMVR, TTVR or surgical valve 1 month post d/c if NYHA I-III 3 months post d/c if NYHA I and LVEF ≧ 50% replacement Updates provide new recommendations for TAVI, TEER, TMVR, TTVR Category Private Car Commercial Arrhythmia Private Car Commercial Driver Driver (Truck, Bus) (Truck, Bus) Sinus node dysfunction No impaired LOC: OK to drive Impaired LOC or high 1 week post implant Impaired LOC/symptomatic pauses: NO grade AV block DRIVING until PPM No impairment in First degree, Wenckebach, OK to drive unless history of impaired LOC LOC/high grade AV OK to drive isolated LBBB, LAFB, LPFB, Pace- block RBBB, bifasicular block maker Generator change Second degree type II, NO DRIVING until PPM (also applies for ICD OK to drive alternating BBB, 3rd degree Exception: congenital 3rd AVB (only private driving) AVB restricted if impaired LOC) Lead upgrade/revision 1 week post implant if history SVT/AF/AFL No impaired LOC: OK to drive (also applies for ICD of impaired LOC/high grade AV Impaired LOC: NO DRIVING until treated private driving) block VF (no reversible causes) 3 months NO DRIVING Otherwise OK to drive VT/VF due to reversible NO DRIVING until underlying cause Primary prophylaxis 1 week post cause (MI, drug, etc.) treated implant Hemodynamically unstable VT or impaired LOC 3 months Secondary prophylaxis, impaired 3 month VT with structural heart ICD NO DRIVING disease and no impaired 3 months NO DRIVING LOC LOC, no ICD Secondary prophylaxis, no 1 week VT with structurally normal 1 week if well impaired LOC heart (idiopathic VT) controlled Category Private Car Commercial Driver (Truck, Bus) CCS 2023 Fitness to ICD shock or therapy, impaired 3 months Drive Guidelines LOC or disabling Category Private Car Commercial ICD shock or Driver ICD therapy, NO 1 week (Truck, Bus) therapy NO DRIVING impaired LOC or Single/recurrent OK to drive disabling vasovagal syncope Inappropriate ICD No restriction Reversible cause 1 week 1 month therapies (orthostatic, Electrical storm (3 3-6 months after dehydration) or Syncope avoidable trigger or more VT/VF event (expert re- events in 24h) evaluation) (micturition) No high risk OK to drive Single unexplained 1 week 12 months features syncope Hyper- High risk Asymptomatic: Recurrent unexplained 3 months 12 months trophic features** OK to drive syncope cardio- Tachy/brady/device Refer to respective arrhythmia or myopathy Syncope: 3 NO DRIVING syncope device recommendation months Prior sustained 3 months **High risk features: think ICD recommendations i.e. wall ventricular thickness >30mm, unexplained syncope, apical aneurysm, arrhythmia LVEF 45 have 2X rate of diabetes First Nations peoples 6X more likely to suffer alcohol-related death, 3X more likely to suffer drug related death Suicide rate of First Nations communities >2X that of total Canadian population – 5-6X more likely for youth 19. We call upon the federal government, in consultation with Aboriginal peoples, to establish measurable goals to identify and close the gaps in health outcomes between Aboriginal and non-Aboriginal communities, and to publish annual progress reports and assess long term trends. Such efforts would focus on indicators such as: infant mortality, maternal health, suicide, mental health, addictions, life expectancy, birth rates, infant and child health issues, chronic diseases, illness and injury incidence, and the availability of appropriate health services. 20. In order to address the jurisdictional disputes concerning Aboriginal people who do not reside on reserves, we call upon the federal government to recognize, respect, and address the distinct health needs of the Métis, Inuit, and off- reserve Aboriginal peoples. 50  TRC Healthcare Calls to Action 21. We call upon the federal government to provide sustainable funding for existing and new Aboriginal healing centres to address the physical, mental, emotional, and spiritual harms caused by residential schools, and to ensure that the funding of healing centres in Nunavut and the Northwest Territories is a priority. 22. We call upon those who can effect change within the Canadian health-care system to recognize the value of Aboriginal healing practices and use them in the treatment of Aboriginal patients in collaboration with Aboriginal healers and Elders where requested by Aboriginal patients. 23. We call upon all levels of government to: i. Increase the number of Aboriginal professionals working in the health-care field. ii. Ensure the retention of Aboriginal health-care providers in Aboriginal communities. iii. Provide cultural competency training for all healthcare professionals. 24. We call upon medical and nursing schools in Canada to require all students to take a course dealing with Aboriginal health issues, including the history and legacy of residential schools, the United Nations Declaration on the Rights of Indigenous Peoples, Treaties and Aboriginal rights, and Indigenous teachings and practices. This will require skills-based training in intercultural competency, conflict resolution, human rights, and anti-racism. 51  Education and Support Physicians should learn more per TRC calls to action. INTERESTED IN READING MORE AS AN INTERNIST? THIS WEBSITE THROUGH THE NORTHERN ONTARIO SCHOOL OF MEDICINE HAS A DECENT COMPENDIUM OF OPEN- ACCESS REFERENCES https://www.nosm.ca/education/rehabilitation-studies/resources/indigenous-health-learning-resources INDIGENOUS MENTAL HEALTH SUPPORTS INDIGENOUS MENTAL HEALTH SUPPORTS The National Indigenous Residential School Crisis Line 24-hour crisis support line 1-866-925-4419 for Residential school students and their families Hope for Wellness support for any First Nation, Metis or Inuit 1-855-242-3310 /online chat at https://www.hopeforwellness.ca/ 52  CARDIOLOGY December 2, 2023 Dr. Michael Ruiz www.internalmedicinereview.ca © Internal Medicine Review 2024  Guiding Principles Broad strokes: Help symptomatic patients feel better Help patients live longer Identify and treat risk factors Practice evidence-based medicine RC tips: Use Canadian Guidelines (CCS) when possible Do not worry about understanding advanced cardiovascular techniques (ablation, angiography, etc.) Be safe!  Outline ACS Acute Coronary Syndrome 1. Coronary artery disease CRT (D) Cardiac Resynchronization Therapy (with Defibrillator) vs. (Pacing only) vs. (P) 2. Heart failure / cardiomyopathy CCTA Coronary CT angiography 3. Valvular heart disease DAPT Dual Antiplatelet Therapy (ASA + clopidogrel or prasugrel or ticagrelor) EST Exercise Stress Test 4. Aortopathy METs Metabolic Equivalents 5. Pericardial disease DOACs Direct Oral Anticoagulants (ex apixaban, dabigatran, rivaroxaban) NSTEACS Non ST Elevation Acute Coronary Syndrome 6. Arrhythmias and implantable cardiac OAC Oral Anticoagulants (Includes VKA, DOAC) devices OMT Optimal Medical Therapy 7. Peripheral arterial disease POBA Plain Old Balloon Angioplasty PCI Percutaneous Coronary Intervention VKA Vitamin K Antagonist (warfarin) NB. ECGs will be self study online SAPT Single Antiplatelet Therapy (ASA OR Clopidogrel) SPECT Single photon emission computed tomography Coronary Artery Disease Key resources: CCS 2014 Guidelines – Diagnosis and management of stable ischemic heart disease ACC/AHA 2023 Guidelines – Chronic CAD  Coronary Artery Disease (CAD) Two major presentations: Chronic stable CAD 2014 CCS guidelines on stable ischemic heart disease 2023 ACC/AHA Guideline on Management of Patients with Chronic Coronary Disease Acute coronary syndromes Various CCS/ACC/AHA guidelines on ACS, antiplatelets  How Do Patients Present? Ischemic cascade – with increasing ischemic time: 1. Blood flow changes (can be seen on myocardial perfusion) 2. Diastolic, then systolic dysfunction (wall motion abnormalities) 3. ECG changes 4. Symptoms 5. Myocardial necrosis  Diagnostic Tests for CAD Functional STRESS: pick exercise whenever possible! Non-invasive stress tests: – Provides prognostic info: e.g. duration of exercise, METs – STRESS = exercise, – Not possible if physical limitations or contraindications drugs (inotropes, (e.g. critical aortic stenosis) vasodilators) – TEST = ECG, ECG+echo, TEST: consider functional imaging (e.g. nuclear) if: ECG+nuclear – Cannot accurately assess for ischemia on ECG LBBB, paced rhythm, preexcitation, significant ST changes at Structural rest à the ECG is not interpretable in these cases – RBBB interpretable generally – Coronary angiography – Need specific anatomic correlation (e.g. prior – CT coronary revascularization) angiography  Able to exercise and no contraindications? Principles of Non- YES NO Invasive ECG Normal à Exercise Stress TEST ECG Abnormal ECG normal or abnormal Testing NO LBBB or V- Paced LBBB or V paced LBBB or V rhythm rhythm No LBBB or V paced paced rhythm Rhythm Exercise Cardiac CT myocardial Exercise ECHO Vasodilator Vasodilator myocardial myocardial Angiography perfusion Image perfusion imaging perfusion imaging Dobutamine or vasodilator Adapted from 2014 echo CCS – Stable Ischemic Heart Disease  Absolute Contraindications to EST Acute MI (within 2 days) Mnemonic: Ongoing unstable angina I – Inflammation Uncontrolled hemodynamically-significant arrhythmia D – Dissection O – Ongoing angina Active endocarditis Symptomatic severe AS N – No consent O – Ongoing MI Decompensated heart failure T – Thrombosis Acute PE, pulmonary infarction, DVT S – Severe AS Acute myocarditis, pericarditis T – Technical issues Acute aortic dissection R – Rhythm E – Endocarditis Physical limitations S – Systolic dysfunction S – Slow  EST Results Positive Negative Equivocal Uninterpretable Maximal vs. submaximal test – Patient should reach 85% of age predicted maximum heart rate – (Max HR = 220 – age)  EST Results Positive test High risk features* – ≥ 1mm STE – Duke Treadmill Score -11 or less – ≥ 1 mm STD (horizontal or – 120, drop in BP >10, drop below baseline] – Ventricular arrhythmia 2013 AHA – Exercise standards for testing and training 2014 CCS – Stable Ischemic Heart Disease  Myocardial Perfusion Imaging Radioactive tracer (e.g. 99mTc) is used that distributes into myocardium proportionally with blood flow SPECT imaging detects decay of tracer Stress = exercise vs. pharmacologic (e.g. dipyridamole) – Pharmacologic stress based on coronary perfusion mismatch after vasodilation dipyridamole (aka persantine) most commonly used for nuclear stress, less commonly adenosine Dobutamine used commonly for stress echocardiography – Diseased coronary vessels are already maximally dilated and develop perfusion mismatch – False negatives can be seen: Drug interactions with dipyridamole (caffeine, theophylline – hold before test!) Severe flow limiting triple vessel or left main disease (“balanced” ischemia so no perfusion mismatch detected) Consider as a potential first-line test if patient cannot complete ECG stress test Contraindications: active or severe asthma/COPD, as dipyridamole can cause bronchospasm – Reversal agent for dipyridamole is aminophylline Coronary CT Angiography (CCTA) NB. CCTA is not the same as a Coronary Artery Calcium (CAC) Score from CT. - CAC scoring is recommended for further risk stratification of intermediate risk (FRS 10-19%) asymptomatic patients aged > 40 who are not candidates for statin based on other risk factors - Can consider CAC scoring for low risk patients with family hx premature CV Dz and genetic dyslipidemia - CAC score > 100 is basically a statin indicated condition; start therapy regardless of FRS  Coronary CT Angiography (CCTA) Procedure specifics: – Low dose CT with beta blockade +/- IV nitro given (HR target 24h post ACS Stopping P2Yi prior to CABG – Limited evidence… “multidisc team” to decide, hold 2-7d pre-op Suggest hold Ticagrelor 2-3 days rather than 5-7d [weak, conditional] Postop Antiplatelet Regimen – Off-pump – favour DAPT, with ASA + ticagrelor/prasugrel over ASA + Clopidogrel – On-pump – favor SAPT – AFIB? – consider OAC monotherapy We think this is beyond scope of GIM – usually our exam questions pertain to NON CARDIAC SURGERY! 31  The Second Antiplatelet… Nuances Ticagrelor is contraindicated if history of: – intracranial hemorrhage – active pathological bleeding – moderate-severe hepatic impairment – combinations with CYP34A inhibitors (ketoconazole, clarithromycin, ritonavir) – Should consider avoiding in patients with evidence of heart block or bradycardia. – Dose: 180mg load then 90 mg bid x 12 months then 60mg bid thereafter Prasugrel is contraindicated if: – active bleeding – prior TIA/stroke [even ISCHEMIC stroke] – hypersensitivity reaction – Dose: 60mg load then 10mg daily (reduce to 5mg if 24h expected before cath, give second antiplatelet – Elective angiogram: do not routinely treat with second antiplatelet  CCS 2023 Antiplatelet Guideline: AFIB + Antiplatelets CCS Antiplatelet 2023 N.B. all of these recommendations are weak unless otherwise specified. Align w CCS AFIB guidelines. Antiplatelet and anticoagulation (i.e. patient on OAC for atrial fibrillation) – Dual pathway (clopidogrel+OAC) recommended over previous strategy of triple therapy for 1-30 days in most patients (but the small text says they need to receive 1 dose of ASA at PCI time, so it is like they only received 1 dose of triple therapy) – OAC monotherapy preferred over OAC+aspirin in stable CAD (from the AFIRE trial which showed rivaroxaban+ASA had more bleeding with no reduction on ischemic events compared to rivaroxaban alone)  *NEW* CCS 2023 Antiplatelet guidelines give clear guidance as to who is high risk of bleeding. Meeting High bleeding risk patient 1 major or 2 minor should trigger you to consider a shorter duration or de-escalated regimen of DAPT Need 1 major Or 2 minor: 1. Advanced CKD (eGFR55%, if LV is the left ventricle. severely enlarged (cut off LV end systolic Systolic dysfunction is a dimension >50mm or indexed to body surface devastating consequence area >25mm/m2) of volume loading (which is why it is a class I Moderate AR undergoing other cardiac surgery recommendation to intervene). Volume loading also Class IIb indications for surgery: causes LV dilation through remodeling, Asymptomatic, severe AR with LVEF >55% but hence why LV progressive decline in LVEF on three serial studies enlargement is included in class IIa and IIb to 55-60% or progressive increase in LV dilation indications for (LV end diastolic dimension >65mm) intervention. AHA 2020 Valve  Mitral Stenosis Etiology is almost all rheumatic (other – MAC, radiation, autoimmune … ) – Often associated with AF – OAC with VKA if i) rheumatic MS and AF; ii) rheumatic MS and prior embolic event; iii) rheumatic MS and LA thrombus INVICTUS trial: VKA vs. rivaroxaban in pts with rheumatic heart disease and AF à VKA had ↓ stroke/systemic embolism/MI/death (i.e. DOAC harmful in this setting!) NEJM 2022 – Management considerations for AF and heart rate MS does not like high HRs à loss of diastolic filling time MS does not like AF à loss of atrial kick Severe MS: – MV area ≤1.5 cm2 (very severe = ≤1 cm2) Echo criteria for severe MS in – Pulmonary artery systolic pressure >50mmHg guidelines… but we don’t think – Diastolic pressure half time (PHT) >150 ms you need to memorize! AHA 2014, 2017, 2020 Valve  Mitral Stenosis - Intervention 2 types of interventions – percutaneous vs. surgical Percutaneous mitral balloon commissurotomy (PMBC) indicated if (Class I): Severe, symptomatic MS + favourable valve anatomy + can be performed at a “Comprehensive Valve Centre” – CONTRAINDICATED if: i) LA thrombus (need preop TEE) ii) >moderate MR MV surgery (commissurotomy +/- repair OR replacement) indicated if (Class I): Severe, symptomatic MS + acceptable surgical risk + contraindicated/failed PMBC Severe MS and other cardiac surgery planned AHA 2014, 2017, 2020 Valve  BONUS Read on own Mitral Stenosis - Intervention Percutaneous mitral balloon commissurotomy (PMBC) is reasonable if (Class IIa)*: An obstructed – Asymptomatic, severe MS with pulmonary hypertension (PA systolic mitral valve leads pressure > 50mmHg by echocardiography or right heart catheterization) to LA dilation, atrial arrhythmias and pulmonary Percutaneous mitral balloon commissurotomy (PMBC) can be hypertension. considered if (Class IIb)*: – Asymptomatic, severe MS with new atrial fibrillation Therefore, think of pulmonary – Asymptomatic, severe MS with mean gradient >15 mmHg or wedge hypertension and pressure >25 mmHg with exercise atrial fibrillation – Highly symptomatic patients (NYHA III-IV) with severe MS with unfavourable as the “end anatomy or high risk for surgery (as a palliative attempt to try to relieve organ” effects of symptoms) mitral stenosis! *All recommendations require the PMBC be performed at a “Comprehensive Valve Centre”. PMBC remains contraindicated if LAA thrombus or moderate or more MR 93  Mitral Regurgitation Acute MR – VERY unstable patients – Ischemia à papillary muscle dysfunction – Chord rupture à patients with mitral valve prolapse may rupture a chord acutely, leading to a flailing mitral valve leaflet acute severe MR – Endocarditis – Trauma Chronic MR – PRIMARY (“degenerative”) à is the disease Valve leaflet (MVP [myxomatous, fibroelastic deficiency], rheumatic) Annulus (calcification) Chordae (trauma, infection, idiopathic) Papillary muscle (trauma) – SECONDARY (“functional”) à is the consequence Dilated or ischemic cardiomyopathy -> leaflet tethering (being pulled towards the apex) + annular dilatation -> leaflet malcoaptation leading to regurgitation Severe MR is defined using specific echocardiographic parameters that you should not need to know  Mitral Regurgitation - Intervention PRIMARY MR – “the goal of therapy is to correct MR before onset of LV systolic dysfunction” Class I indications for surgery (repair when possible vs. replacement) for PRIMARY MR: Severe, symptomatic 1o MR irrespective of LVEF Severe, asymptomatic 1o MR + LV systolic dysfunction (LVEF ≤ 60%, LVESD ≥ 40mm) AHA 2014, 2017, 2020 Valve  BONUS Read on own Mitral Regurgitation - Intervention Class IIa indications for for PRIMARY MR (reasonable): Asymptomatic patients with severe MR with preserved systolic function (LVEF ≥60%, LVESD 95% success and 12mmHg) ventricular interdependence) lack of ITP transmission) interdependence) Other features Beck’s triad (low BP, high JVP, Pericardial knock (rapid early Manifestations of systemic muffled heart sounds) diastolic filling) +/- friction rub disease (amyloid, sarcoid)  Arrhythmias Key Resources: +++ CCS AF Guidelines [NB. Most recent = 2020 update] CCS 2020 Syncope Update ACC/AHA 2018 Pacing Guidelines ESC 2021 Pacing Guidelines CCS VT Guidelines ACLS Guidelines  Screening for Atrial Fibrillation (AF) General Population – pulse-based screening or rhythm-based screening at all routine health assessments in people >65yrs – follow-up with ECG assessment if “irregularly irregular” Cardiac Implantable Electrical Device (PPM, ICD) – interrogate all high atrial rate episodes for possible AF Non-lacunar Embolic Stroke of Unknown Source – ”at least 24h of ambulatory ECG monitoring” Longer monitoring if AF is still suspected but not proven CCS 2020 AF Update  AF Etiology & Initial Investigations Major Guideline: CCS 2020 CCS – SAF Scale – Symptoms of AF Major Considerations: Class 0 Asymptomatic Always look for an etiology/precipitant Class I Minimal symptoms or 1 episode without syncope or CHF (EtOH, drugs, withdrawal, ischemia, PE, Class II Symptoms have minimal effect: valves, thyroid disease, OSA, infection, sleep - Mild awareness if in persistent/permanent AF deprivation, acute pulmonary disease … ) - Rare episodes (“less than a few per year”) in those Basic Workup for new AF: w/ paroxysmal AF. Document rhythm Class III Symptoms have moderate effect on QOL: ECHO – assess LV size and function, LA size, valve.. - Moderate awareness most days with CBC, lytes (Ca, Mg), Cr, Coags, TSH for all persistent/perm AF LFT before amiodarone prescription - More common episodes (”more than every few A1C, FBG, Fasting lipid profile as part of comprehensive months”) or more severe symptoms in pts with cardiac risk assessment paroxysmal AF Always assess patient AF-related symptoms and quality of life (CCS-SAF), assess patients Class IV Symptoms have severe effect on QOL: - Syncope due to AF and / or with AF for frailty, cog impairment, - CHF due to AF and / or dementia, depression - Unpleasant symptoms in pts with persistent/perm AF and / or - Frequent and highly symptomatic episodes in pts w CCS 2020 AF Update paroxysmal AF  AF: Prevention and Treatment Major Considerations cont’d: Prevention = modifiable risk factor management Achieve rate control with b- blocker, CCB, or digoxin AF with pre-excitation (WPW): àDC cardioversion (or procainamide) Rhythm control preferred if QoL impaired (symptomatic despite rate control) or hemodynamically unstable (DC cardioversion) This cutoff of 130/80 Is not mentioned in the CCS text anywhere, only in this figure! We suggest just go with HTN CCS 2020 AF Update Canada guidelines for resting BP target. CCS 2020 AF Update  What about Atrial Flutter (AFL)? “It is recommended that patients with Atrial Flutter be stratified and treated in the same manner as patients with atrial fibrillation.” 126  Anticoagulation in AF/AFL DOACs are 1st line for almost everyone – VKA (i.e. warfarin) should be used instead of DOAC for valvular AF (CCS 2016, 2018 and 2020 definition): Mechanical heart valves Rheumatic mitral stenosis Moderate-severe non-rheumatic mitral stenosis – Warfarin should also be considered (class IIa) in patients with new onset AF ≤ 3 months post-valve replacement (surgical or percutaneous) *NEW* FRAIL-AF (Circulation, 2023) looked at elderly (>75) frail patients with AF who were already on VKA and randomized to change to DOAC vs stay on VKA. Surprisingly, more bleeding was observed in those who were switched to DOAC (15.2%) compared to those who continued VKA (9.4%), trial stopped early. – Criticisms – small trial (n=1330), bleeding events were self reported and the primary outcome was driven by minor bleeding, not major bleeding. No formal guideline recommendations have incorporated this trial. – No difference in ischemic/embolic events – Take Away #1 – if elderly frail patient stable on VKA can continue – Take Away #2 – caution in extrapolating results of other RCTs to populations excluded from enrolment (frail elderly) CCS 2020 AF, CCS 2020 Valve  Anticoagulation in CKD/ESRD Calculate CrCl using Cockroft – Gault at baseline, and REFERENCE: Dosing per manufacturer at least annually: Apixaban Stage 3 CKD (eGFR >30) – A/C as usual – 5mg PO BID – 2.5 mg PO BID if 2/3: ≥80 years, ≤ 60kg, creatinine Stage 4 CKD (eGFR >15 75 years or eCrCl 30-49 mL/min – “The CCS recommends that a DOAC is preferred over VKA” Edoxaban – “Apixaban and rivaroxaban are approved for – 60 mg PO daily use with stage 4 CKD” – 30 mg PO daily if CrCL 30-50 mL/min, ≤ 60kg, or concomitant use of potent P-glycoprotein inhibitors Stage 5 CKD (eGFR 0 à OAC only – Prefer DOAC > VKA *STABLE CAD = no PCI or ACS in preceding 12 months CCS 2020 AF Update  (2a) AFIB + PCI (elective or ACS) Individualize based upon thrombotic risk LOW RISK thrombotic events HIGH RISK thrombotic events or Elective PCI (no ACS) ACS with PCI CHADS65 = 0 à DAPT CHADS65 = 0 à DAPT – DAPT for 6-12 months per CCS 2018 Antiplatelet Guidelines for non-AF patients CHADS65 >0 à “Dual Pathway” CHADS65 >0 à “Triple Therapy”x1-30d – SAPT with a P2Y inhibitor* + OAC for at least 1 month, up to 12 months after PCI, THEN then OAC alone “Dual Pathway Therapy” = clopidogrel + OAC up to 12 months post PCI THEN OAC only **NEW** CCS 2023 Antiplatelet Guidelines says for PCI and need for OAC, dual pathway is recommended over triple therapy but specifies they receive 1 dose of ASA with PCI. Therefore it is as if they had “1 day of triple therapy.” If asked in an exam situation, minimizing triple therapy (1-30 days) or going straight to dual pathway would be guideline recommended durations. Talking with the interventionalist would also be an important step (i.e. how complex was the PCI). *P2Y inhibitor = Pick CLOPIDOGREL – lower bleeding risk CCS 2020 AF Update Who is HIGH RISK Post-Elective PCI? Mitigate bleeding risk: Avoid prasugrel/ticagrelor – that’s why they say clopidogrel in guideline table Consider PPI Avoid other NSAIDs if VKA target INR 2-2.5 CCS 2020 AF Update  (2a) AFIB + ACS – NO PCI /stent Individualize based upon thrombotic risk CHADS65 = 0 à DAPT = Dual Antiplatelet Therapy (ASA + P2Y inhibitor) CHADS65 > 0 à “Dual Pathway Therapy”: clopidogrel + OAC [apixaban1] for 1 to 12 months post ACS THEN OAC only 1TIP – the only OAC studied after ACS without PCI is apixaban 5mg po bid. This is favoured in wording of guidelines for this scenario with clopidogrel. CCS 2020 AF Update  Prescribing notes – not all OAC the same dose in dual pathway, triple therapy: The OAC component of dual pathway regimens includes: normal dose edoxaban, apixaban, dabigatran BUT rivaroxaban only 15 mg PO daily (10 mg in patients with CrCl 30-50 mL/min). – A DOAC is preferred over warfarin, however if warfarin is to be used the lower end of the recommended INR target range is preferred. All patients should receive a loading dose of ASA 160 mg at the time of PCI (if previously ASA-naïve). The OAC component of triple therapy regimens includes: warfarin daily, rivaroxaban 2.5 mg PO BID, or apixaban 5 mg BID (reduced to 2.5 mg if they met two or more of the following dose reduction criteria: age > 80 years of age, weight < 60 kg, or Cr > 133 μmol/L). – A DOAC is preferred over warfarin, however if warfarin is to be used the recommended INR target is 2.0-2.5. All patients should receive a loading dose of ASA 160 mg at the time of PCI (if previously ASA-naïve). Thereafter, ASA may be discontinued as early as the day following PCI or it can be continued longer. The timing of when to discontinue ASA will depend on individual patient’s ischemic and bleeding risk. The dose of OAC beyond one year after PCI should be standard stroke prevention doses. A combination of an OAC and single antiplatelet therapy may be used only in highly selected patients with high-risk features for ischemic coronary outcomes, and who are also at low risk of bleeding CCS 2020 AF Update  CCS 2020 AF Update AF – OAC in Special Populations Liver Disease We recommend that OAC not be routinely prescribed in Child-Pugh class C or liver disease associated with significant coagulopathy Cancer Individualize OAC treatment in pts with active cancer. Consider DOAC> VKA. Congenital Heart Disease OAC for most patients with AF and HCM OAC if CHADS65 risk factors Frail Elderly OAC for most frail elderly – individualizing recommendations if high risk bleed Secondary Atrial Fibrillation No OAC =clearly provoked by transient/ Exceptions: patient’s underlying ‘abnormal substrate’ and risk for recurrence reversible risk factor such as estimated to be high and for “most patients during acute thyrotoxicosis until severe sepsis, thyrotoxicosis euthyroid state is restored” Pregnancy No DOACs (cross placenta). Consider LMWH, Warfarin (Tri2-3) in unique (2021 CCS Pregnancy Heart circumstances (see OB Med lecture for more details). Anticoag should be considered Disease Update) for pregnant women with AF and (1) structural heart disease or (2) no structural heart disease but CHADS >=1 High atrial events (i.e. PACs) *NEW* NOAH-AFNET6 trial looked at patients with mean CHA2DS2VASC 4 and high WITHOUT AF atrial events (i.e. PACS) but no AF and started them on edoxaban vs. placebo. NO DIFFERENCE in stroke/systemic embolism. Don’t start DOACs for PACS! Cardio- version of AF DOAC preferred CCS 2020 AF Update  MCQ #4 2024 A 68yF is investigated for palpitations. She is a retired nurse and noticed that for the last two years her HR is irregularly irregular. 48h Holter reveals she is in Afib throughout the study, 95% of the time rates controlled 100 msec in TCA overdose. If QRS narrows then start bicarb infusion. b) Administer physostigmine to counteract the anticholinergic toxicity – contraindicated in TCA overdose due to the risk of cardiac arrest. c) Give Dilantin for seizure prevention – no indication for seizure prevention, but even for seizure treatment, avoid Dilantin due to the sodium channel blockade that could worsen cardiac arrhythmias. Mainstay is benzodiazepines for seizures and agitation. d) Cardiovert the patient – not indicated at this point, especially if patient responds to bicarbonate therapy. 122  BONUS Read on own MCQ #4 (2023) A 45 year old male with morbid obesity is admitted for respiratory failure secondary to pneumonia. He has a prolonged course on the ventilator and underwent tracheostomy 5 days ago. He becomes agitated and today he pulls out his trach. What do you do? a) Reinsert the trach b) Orotracheal intubation c) Crichothyroidotomy d) Place on nasal prongs and monitor 123  BONUS Read on own MCQ#4 (2023) What do you do? a) Reinsert the trach – do not reinsert a trach, unless the tract is mature (7-10 days minimum). This could lead to subcutaneous emphysema when placed on the vent and rapid respiratory/cardiac arrest. b) CORRECT - Orotracheal intubation – this is the first step, intubate from above to secure the airway. c) Crichothyroidotomy – consider this if unable to intubate or ventilate. d) Place on nasal prongs and monitor – not recommended for a patient who failed previous extubation and was unable to wean from the vent. 124  BONUS Read on own MCQ #5 (2023) A 25 year old female presents with an acute Tylenol overdose. She ingested 8.5 g four hours before presentation. She is asymptomatic currently, and was given activated charcoal. Her GCS is 15 and she is vitally stable. Her exam is remarkable for mild right upper quadrant tenderness. Her labs are unremarkable, AST and ALT are within normal limits. Her Tylenol level is above the treatment line on the RM nomogram. She is started on a NAC infusion. Thirty minutes into the infusion she develops urticaria and flushing. The infusion is stopped, she is given benadryl and the reaction subsides. What is the best course of action? a) Do not restart the infusion and consult Nephro for hemodialysis b) Switch to PO NAC c) Reduce the dose by half and uptitrate if the infusion is tolerated d) Restart the infusion and monitor for airway compromise or signs of anaphylaxis 125  BONUS Read on own MCQ #5 (2023) What is the best course of action? a) Do not restart the infusion and consult Nephro for hemodialysis – there is no role for hemodialysis in Tylenol overdose if you are able to continue with NAC therapy. Hemodialysis may be considered to lower Tylenol concentrations if NAC is not available or if there is a concurrent renal failure. b) Switch to PO NAC – no indication to switch routes of administration. c) Reduce the dose by half and uptitrate if the infusion is tolerated – dose reduction is not recommended by guidelines, instead you should continue the recommended NAC protocol dosing regimen. d) CORRECT - Restart the infusion and monitor for airway compromise or signs of anaphylaxis – this is appropriate to optimize Tylenol toxicity treatment and for liver protection. 126  BONUS Read on own MCQ #6 (2023) A 66 year old obese male is admitted to the ICU with acute hypercarbic respiratory failure secondary to a severe COPD exacerbation. He presents with a CO2 of 85, and with this has a GCS of 10. He is started on steroids, routine puffers, and trialed on BiPAP, and after 2 hours his GCS is 8 and his CO2 has climbed to 105. The decision is made to intubate the patient. His initial vent settings are: ACPC 14/5, 40% FiO2, RR 18. Peak pressures are 35 cm H2O, plateau pressures are 20 cm H2O, driving pressure is 15 cm H2O, and tidal volume is 8 ml/kg. You are called to his bedside 3 hours later because the patient has acutely desaturated, and is requiring an FiO2 of 80%. His SpO2 is now 85%. How would you advise adjusting the ventilator settings to improve his oxygenation? a) Increase the FiO2 to 100% b) Increase the respiratory rate to 25 breaths per minute c) Switch to volume control ventilation d) Increase the PEEP to 10 cm H2O 127  BONUS Read on own MCQ #6 (2023) How would you advise adjusting the ventilator settings to improve his oxygenation? a) Increase the FiO2 to 100% - this would not be recommended before optimizing the PEEP due to the negative effects of hyperoxia on lung tissue (increase in free radicals). b) Increase the respiratory rate to 25 breaths per minute – this would increase minute ventilation, which would improve ventilation (CO2 clearance), but would not impact oxygenation. c) Switch to volume control ventilation – this would be recommended in lung protective ventilation (for ARDS), but in other clinical situations pressure control is appropriate, unless concern of ventilator dysynchrony. d) CORRECT Increase the PEEP to 10 cm H2O – this would be indicated to optimize oxygenation by improving recruitment and reducing atelectasis to optimize gas exchange. Likely in this scenario the patient de-recruited from having too little PEEP in the context of his underlying obesity and COPD. 128  MCQ 7 (2024) 45 year old patient is admitted to the general internal medicine ward with acute respiratory failure secondary to influenza. Their medical history includes hypertension. They were initially managed with conventional oxygen therapy, with nasal prongs 4L/min. On repeat assessment their hypoxemia is worsening with O2 sats 85% on non- rebreather mask at 12L/min and they have increased work of breathing. They are following commands and speaking in short sentences. VBG shows pH 7.42, CO2 35, Bicarb 24. What is the best next step in management? 1. Non-Invasive Ventilation 2. High-Flow Nasal Cannula 3. Intubation 4. Proning 5. Hydrocortisone 100 mg IV 129  MCQ 7 (2024) 1. Non-Invasive Ventilation Non-invasive ventilation should be used for hypoxemia secondary to cardiogenic pulmonary edema, and can be considered for acute respiratory failure in patients with chest trauma, immunocompromised state, post-operative, palliative with dyspnea. There is no recommendation made for de novo respiratory failure without these conditions. 2. High-Flow Nasal Cannula Strong indication for hypoxemic respiratory failure OVER conventional oxygen therapy 3. Intubation There is no strong indication for intubation yet. Airway is protected (patient is talking, alert) and work of breathing/hypoxemia may improve on HFNC. 4. Proning Self proning can be considered for hypoxemia in setting of covid in non-intubated patients. However, HFNC would be used first. 5. Steroids Steroids have a benefit in treating Severe COMMUNITY ACQUIRED PNEUMONIA (data covered in ID lecture) and with COVID 19 (Dexamethasone) – however can actually be harmful (more nosocomial infection, possibly more mortality) with influenza. Even if you didn’t know this data, in this setting next best step (ABCs!) is to administer more oxygen if you were choosing best answer on MCQ. 130  MCQ 8 (2024) 65 year old patient is admitted to the ICU after an unwitnessed out-of-hospital cardiac arrest secondary to fentanyl overdose. It is now 60hrs since the arrest. CT head shows diffuse grey- white matter loss in keeping with a hypoxemic-ischemic brain injury, with cerebral edema and tonsillar herniation. Post-cardiac arrest management included therapeutic hypothermia targeting 35-36 degrees C. Passive rewarming has started and the current core temperature is 35.6 degrees C. The patient was sedated with propofol and ketamine which were stopped 24hrs after the cardiac arrest. No neuromuscular blockers were used. MAP is currently 70 with vasopressin, ABG showing pH 7.33, PaCO2 45, lactate 1.7. Bicarb 24. Further labs show Na 150, K 3.4, Cr 140, Urea 15, Calcium 2.1, Mg 0.8, Phosphate 0.7, Bilirubin 20, ALT 60, ALP 80. Which of the following would prevent death by neurological criteria assessment? 1. Time since cardiac arrest 2. Core temperature 3. Metabolic derangement 4. Shock 5. Sedative medication 131  MCQ 8 (2024) 1. Time since cardiac arrest Updated canadian guidelines 2023 state to wait at least 48hrs since cardiac arrest before completing DNC assessment. 2. Core temperature Core temperature must be ≥36 degrees C in latest guidelines (previously 34) before completing DNC assessment 3. Metabolic derangement Metabolic derangements that are severe should be corrected before completing DNC assessment. However, none of the metabolic derangements in this case would be considered severe enough. 4. Shock Shock is resuscitated in this case with vasopressor support and a normal lactate. Only un-resuscitated shock prevents DNC assessment (i.e. high lactate, end organ ischemia/dysfunction, MAP < 65 despite vasopressors). 5. Sedative medication New guidelines suggest waiting 5 half lives of medications. 60hrs would be long enough for fentanyl (1/2 life approx 4-7hrs) and ketamine/propofol (stopped approx 40hrs ago). 132  MCQ 9 (2024) 80 year old patient presents to the emergency department with nausea and vomiting secondary to a small bowel obstruction. Past medical history includes chronic pain, depression, cholecystectomy. Home medications are citalopram, hydromorphone contin, senna. The patient undergoes an urgent laparotomy with resection of adhesions for management of the small bowel obstruction. They are admitted to the ICU for post-operative management. Issues during the ICU stay include post-operative ileus, delirium and pain. ICU medications include hydromorphone CR, IV fentanyl, IV gravol, IV metoclopramide, lansoprazole, citalopram, dalteparin 5000 u sc daily. On post-operative day 3 the patient develops a temperature of 39 degrees C. Vitals shows BP 130/80, HR 110, RR 20, Sats 96% 2L NP. Examination shows pupils 5mm and equal, diaphoresis, agitation, lower limb rigidity with brisk reflexes, ankle clonus x 12 beats bilaterally. Which syndrome most likely explains the findings? 1. Sympathomimetic toxidrome 2. Anti-cholinergic toxidrome 3. Serotonin syndrome 4. Neuroleptic malignant syndrome 5. Malignant hyperthermia 133  MCQ 9 (2024) 1. Sympathomimetic toxidrome No inciting cause. Rigidity not expected. Patient would have significant hypertension. 2. Anti-cholinergic toxidrome Excessive levodopa could cause this, but would expect dilated pupils. Does not explain hypertonia. 3. Serotonin syndrome Fentanyl and citalopram (SSR) could cause serotonin syndrome; addition of metoclopramide to the mix can worsen risk of serotonin syndrome in patients on SSRIs!! He has fever, rigidity, hyperreflexia and clonus so this fits the bill. 4. Neuroleptic malignant syndrome There are features of NMS (hyperthermia, rigidity,) and an inciting cause potentially (metoclopramide) – however the hyperreflexia doesn’t fit with this syndrome and is better explained by serotonin syndrome. 5. Malignant hyperthermia Too long since volatile anaesthetic. This would occur minutes/hrs after exposure. 134  MCQ 10 (2024) A patient has been admitted to the intensive care unit after a motor vehicle collision. Their injuries include a severe traumatic brain injury (TBI), rib fractures, splenic laceration, and facial fractures including an orbital fracture with disruption of the ocular muscles resulting in fixed abduction of the right eye. The patient remains GCS 3 48hrs into admission with CT evidence of severe cerebral edema, mass effect and herniation. Examination reveals no brainstem reflexes. No further options are available for management of the TBI. Review of the chart shows no confounders to death by neurologic criteria (DNC) assessment. What is the appropriate next step? 1. Wait a further 24hrs hours before completing DNC assessment 2. Order an MRI 3. Proceed with DNC assessment 4. Order a CTA head and neck as an ancillary test 5. Order SSEPs 135  MCQ 10 (2024) 1. Wait a further 24hrs hours before completing DNC assessment DNC assessment can occur ≥48 hrs after a cardiac arrest, or earlier if neuroimaging shows a devastating injury. There has been no cardiac arrest and imaging shows a devastating injury so there is no need to wait longer. 2. Order an MRI to characterise the cause of coma MRI is useful in neuroprognostication, but is not an accepted ancillary test 3. Proceed with DNC assessment Cannot proceed with DNC because the ocular injury and persistent lateral abduction prevents assessment of brainstem reflexes. For example, vestibulo-ocular requires assessment of eye movement (nystagmus). 4. Order a CTA head and neck as an ancillary test An ancillary test is required. CTA is an accepted option. 5. Order SSEPs for neuroprognostication SSEPs are useful in neuroprognostication, but is not an accepted ancillary test 136  MCQ 11 (2024) A patient presents 4 hours after an ingestion of an unknown quantity of pills and clear liquid. They are initially confused and agitated, and subsequently become drowsy. Bloodwork shows Na 140, K 4.5, Cl 105, bicarb 21, urea 10, glucose 5, VBG pH 7.30 pco2 40, lactate 2.4, serum etoh 30 mmol/l, plasma osmolality 395, serum/urine ketones positive, acetaminophen 80 micromol/l (upper limit normal < 66, rumack-mathew treatment threshold >800 micromol/l at 6hrs) What is the next best step in management? 1. D10 infusion 2. NAC infusion 3. Dialysis 4. Fomepizole 5. Single Dose Activated Charcoal 137  MCQ 11 (2024) 1. D10 infusion This can be used for salicylate toxicity to prevent cerebral hypoglycemia despite normal serum blood glucose levels. There is no respiratory alkalosis to suggest salicylate toxicity. 2. NAC infusion The acetaminophen level given is below the treatment threshold at this time post ingestion so NAC is not the next best step. In scenarios where the time of ingestion is uncertain or there are risk factors for hepatotoxicity then NAC can still be given. 3. Dialysis Acetaminophen is dialyzable (See EXTRIP for indications), but this scenario is n