CV Flashcards

(118 cards)

1
Q

HF

Types of HF?

A

HFrEF = LVEF ≤ 40%
HFnrEF = LVEF > 40%

Used to be HFpEF, HFmrEF, and HFrEF.

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2
Q

HF

What is HF?

A

Impaired ability of ventricles to fill with (diastole) or eject (systole) blood.

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3
Q

HF

Clinical presentation of HF?

A

Hypotension - hypoxia, fatigue, cyanosis, confusion, chest pain
dyspnea - sudden nocturnal dyspnea, orthopnea, tachypnea, crackles, cough
Systemic congestion - Jugular venous congestion, hepatomegaly, ascites, n/v
peripheral edema - weight gain, abdominal distension

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4
Q

HF

Diagnosis of HF?

A
  1. clinical hx + physical exam
  2. diagnostic workup (ECG, CXR, lab work)
  3. ongoing suspicion of HF
  4. Echo +/- additional diagnostic investigations (natiuretic peptide testing)
  5. likely HF
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5
Q

HF

HYHA Classification?

A

Class I: no limitation of PA, no SOB, fatigue, or heart palpitations w/ ordinary PA.
Class II: slight limitation of PA, sxs w/ PA.
Class III: marked limitation of activity, sxs occur during less than ordinary activity but comfortable at rest.
Class IV: sxs at rest causing severe limitation of activity.

PA = physical activity

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6
Q

HF

Risk factors for and causes of HF?

A

HTN (risk reduced by 50% if HTN is managed), DM, CAD, male (HFrEF), smoking, older age, obesity, DLD, valvular heart disease, tachyarrhythmias, heavy EtOH use, physical inactivity, congenital abnormalities, infections, meds.

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7
Q

HF

Drug causes of HF and HF exacerbations?

A

Fluid retention: NSAIDs, corticosteroids, gabapentinoids, thiazolidinediones, black licorice.
Reduced CO: antiarrhythmic drugs (dronedarone, flecinide, propafenone), CCBs (verapamil, diltiazem), itraconazole, overdose of TCAs, carbamazepine.
Oncology drugs: anthracyclines (doxorubicin), antimetabolites (5-FU), alkylating agents (cyclophosphamide, ifosfamide), taxanes (paclitaxel), IL-2.
Other: clozapine (myocarditis), lithium, sympathomimetics (amphetamines, methylphenidate, cocaine), saxagliptin (incr. risk of HF hospitalizations), hydroxychloroquine, TNFi (infliximab)

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8
Q

HF

Non-Pharm Measures for HF?

A

Salt restriction (< 2-3 g/d)
fluid restriction (< 2L all sources)
No EtOH + smoking cessation
Exercise moderately
monitor weight frequently
immunizations: influenza and pneumo
treat risk factors
PCI/CABG in symptomatic ischemia
ICD if hx of sudden cardiac arrest or ventricular fibrilation

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9
Q

HF

HFrEF pillars of therapy?

A
  1. ARNI or ACEi or ARB
  2. BB
  3. MRA
  4. SGLT2i
    Plus diuretics to releive fluid overload.

ARNI preferred.

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10
Q

HF

Additional drug therapies for HF?

A

Ivabradine: if HR > 70 bpm + NSR
Vericiguat: recent HF hospitalization
Hydralazine-nitrates: black pts on optimal therapy
Digoxin: suboptimal rate control for AF or persistent sxs despite optimized therapy.

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11
Q

HF

How to titrate HFrEF drugs and timeline?

A

Titrate q2-4w to target or to max tolerated dose over 3-6m.

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12
Q

HF

HFnrEF treatment?

A

SGLT2i and MRA, plus diuretic for fluid overload, plus any add ons:
1. GLP1-RA if LVEF ≥ 45% + BMI ≥ 30 mg/m2
2. ARNI (or candesartan): not at risk of hypotension + SBP ≥ 100 mmHg

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13
Q

HF

Role of SGLT2i in HF? Drug(s)?

A
  • HFrEF: improve sxs and reduce HFH + CV mortality regarless of DM status. Best evidence for DAPA and EMPA.
  • HFnrEF: reduce risk of HFH.

HFH = HF hospitalization

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14
Q

HF

HF + SGLT2i PEARLS?

A
  • not used in HF + T1DM
  • hold if sick (dehydrated)
  • if altered kidney fx - avoid starting empa (< 20) and dapa (< 25), may continue
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15
Q

HF

SGLT2i AEs?

A
  • transient eGFR dip (15-25%) (resolves 1-3m)
  • cana has increased risk of lower limb amputation
  • genital mycotic infections
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16
Q

HF

Role of MRA in HF? Drug(s)?

A

Spironolactone, eplerenone, finerenone.
* HFrEF: reduce sxs, CV hospitalizations, and mortality. ONLY Spir/Ep recom.
* HFnrEF: reduce risk of HFH.

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17
Q

HF

HF + MRA pearls?

A
  • monitor renal fx + lytes within 1 week of initiation or dose change, then q3m.
  • avoid initiating if K > 5
  • if altered renal fx - avoid starting Spir/Ep (< 30) and Fin (< 25)
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18
Q

HF

MRA AEs?

A
  • hyperkalemia, d/c if K ≥ 6
  • Spir has anti-antrogen and can cause gynecomastia and impotence
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19
Q

HF

What is an ARNI?

A

Valsartan/Sacubitril - neprolysin inhibitor which increases vasodialtion, and Na excretion.

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20
Q

HF

Role of ARNI in HF? Drug(s)?

A

Valsartan/sacubitril.
* HFrEF: decreases sxs, HFH, and CV death. If newly diagnosed start on ARNI if possible. Acute decomendated on ACEi/ARB should switch to ARNI.
* HFnrEF: reduces HFH in those not at risk of hypotension (weaker evidence)

HFH = HF hospitalizations

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21
Q

HF

HF + ARNI pearls?

A
  • caution K > 5, eGFR < 30, or SBP < 100
  • washout 36h when switching from ACEi to ARNI (not nec. w/ ARB b/c ARB already in)
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22
Q

HF

ARNI AEs?

A
  • hypotension
  • hyperkalemia
  • angioedema
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23
Q

HF

Role of ACEi/ARB in HF? Drug(s)?

A
  • HFrEF: decrease sxs, mortality, and HFH. No clear role in early management of acute/worsening HFrEF, but if MI initiate ASAP.
  • HFnrEF: No evidence for ACEi, Candesartant preferrend when ARNI cannot be used, reduced HFH.

HFH = HF hospitalizations

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24
Q

HF

ACEi/ARB + HF pearls?

A
  • transient decrease in eGFR (up to 30%) when initiating
  • consider ARB when ACEi not tolerated (do not combine)
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25
# HF ACEi/ARB AEs?
* ACEi induced cough - may switch to ARB or ARNI * hypotension, hyperkalemia, h/a * CI in pregnancy
26
# HF Role of loop diuretics in HF? Drug(s)?
Furosemide, bumetanide, ethacrynic acid * HFrEF + HFnrEF: maintain euvolemia and releive congestion (decrease sxs)
27
# HF Loop diuretics + HF pearls?
* consider decreasing or d/c loop diuretics when starting ARNI to prevent symptomatic hypotension or renal dyfx from dehydration * furosemide and bumetanide are sulf-containing - caution in pts w/ sulfa allergies. Ethacrynic acid can be used instead.
28
# HF Loop diuretics AEs?
* hypokalemia, hypomagnesemia, hyponatremia, hypocalcemia, hypertriglyceridemia, hyperglycemia * ototoxicity, photosensitivity, dizziness, urinary frequency
29
# HF Role of GLP1 or Dual GLP1/GIP? Drug(s)?
GLP1 (semaglutide) or GLP1/GIP (tirzepatide) * no specific indication for HFnrEF but can be considered for comorbidities * reduced HFH and improved QOL in patients with LVEF ≥ 45% and BMI ≥ 30 * appears to improve sxs
30
# HF GLP1 and GLP1/GIP + HF pearls?
* semaglutide w/ or w/out meals * do not use tirzepatide w/ DPP4i or GLP1
31
# HF GLP1 and GLP1/GIP AEs?
* n/v/d, injection site rxns * rare: acute pancreatitis, gallbladder disease * decrease gastric emptying
32
# HF Role of BB in HF? Drug(s)?
Bisoprolol, carvedilol * HFrEF: reduces mortality and HFH * HRnrEF: no indication but used to manage comorbidities (e.g. AF) ## Footnote HFH = HF hospitalizations
33
# HF BB + HF pearls?
* start low and increase slowly, double dose q2-4w * avoid abrupt cessation - rebound tachycardia * consider selective agent (bisoprolol) if concomitant reactive airway disease * CI in pts w/ heart block > 1 degree w/out pacemaker - if AV block is present, consider decreasing other AV node-blocking agents (e.g. amiodarone, digoxin)
34
# HF BB AEs?
* may mask hypoglycemia - monitor * transient fluid retention upon initiation or titration
35
# HF Role of ivabradine in HF? ## Footnote Class - HCN channel blocker (Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels)
* HFrEF: recommended in patients with symptomatic HF despite four pillars of medications and with RHR 70+ bpm in NSR. Approved for RHR 77+ in Canada. * HFnrEF: no reccomendation.
36
# HF Ivabradine + HF pearls?
* used in pts who are intolerant to BBs w/ RHR 70+ bpm and in NSR. * AVOID in pts w/ advanced liver disease * tolerated well in elderly patients
37
# HF Ivabradine AEs?
* blurred vision and phosphenes (light rings/spots) - onset w/in 2 months, resolves if stopped. * QT prolongation, bradycardia
38
# HF Ivabradine MOA?
Hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blocker. Sinus node inhibitor - inhibits depolarizing (If) current in the sinus node, **decreasing heart rate without lowering blood pressure or myocardial contractility!!**
39
# HF Role of digoxin in HF?
* HFrEF: releives sxs and reduces HFH in those with HFrEF in NSR who have mod-severe sxs despite four pillars. Also used in pts w/ HFrEF + AF with poor ventricular rate control and/or persistent sxs despite BB optimization. * HFnrEF: no recommendation ## Footnote HFH = HF hospitalization
40
# HF Digoxin + HF pearls?
* serum digoxin levels < 1.2 ng/mL are associated with lower morbidity, though levels should not be used to guide chronic therapy. * increased risk of digoxin toxicity in pts with reduced renal fx, low body weight, and women. * monitor SCr and K with dose increases of digoxin or during dehydrating illness
41
# HF Digoxin AEs?
* atrial and ventricular arrhythmias - risk increases with hypokalemia and reanl function decline * visual disturbances, n/v/d, may cause anorexia
42
# HF Role of vericiguat in HF?
* HFeEF: added to four pillars in patients with worsening HF sxs and HFH in the past 6 m (reduces HFH and mortality - *VIRTORIA*) * NFnrEF: no indication ## Footnote HFH = HF hospitalization
43
# HF Vericiguat + HF pearls?
* indicated in high risk pts that have high rates of hospitalization and risk of mortality * avoid in pts with SBP < 100 mmHg and eGFR < 15 mL/min/m2
44
# HF Vericiguat AEs?
* Hypotension * dyspepsia * nausea * anemia
45
# HF Vericiguat MOA?
Soluble guanylate cyclase (sGC) stimulator which bypasses the need for NO to act as a vasodilator by increasing cyclic GMP production. ## Footnote NO = nitric oxide
46
# HF Role of nitrate/hydralazine in HF? Drug(s)?
Isosorbide dinitrate, hydralazine * HFrEF: vasodilation in those who are unable to tolerate ARNI, ACEi, or ARB due to hyperkalemia, renal dyfx, or other CIs. Also added to four pillars in black pts with HFrEF and advanced sxs. Decrease sxs and mortality. * HFnrEF: no indication.
47
# HF Nitrate/hydralazine + HF pearls?
* avoid with sGC stimulators (vericiguat) due to risk of additive hypotension.
48
# HF Nitrate/hydralazine AEs?
* hypotension * headache * flushing * weakness * lupus like syndrome with hydralazine (less common but serious)
49
# HF what washout period is req. when switching b/w ACEi, ARB, + ARNI?
ACEi to ARNI = 36 hour washout ACEi to ARB = no washout ARB to ARNI = no washout IF angioedema with ACEi, cannot switch to ARNI due to similar risk with ARNI. ARB safe if ACEi caused angioedema (does not interfere with bradykinin metabolism), washout period may be recommended if urgent drug therapy is not req. ## Footnote Washout required due to risk of angioedema
50
# HF Acute decompensation of HF presentation?
* sudden worsening of sxs - dyspnea, swelling, volume overload, fatigue volume overload assessment - * clinically: pulmonary edema, swelling, elevated JVP * objectively: current weight vs dry weight
51
# HF Tx of acute decompensation of HF?
* high dose loop diuretics (to remove excess fluid) * treat underlying cause (if any) * if previously on BB continue, if not start once stable * generally, continue home HF regimen as vitals and clincial context permits
52
# HF HF + pregnancy considerations?
* ACEi, ARB, ARNI, MRA all CI in pregnancy * Ivabradine and SGLT2i should be avoided due to insufficient data * DOC: BB (no atenolol, metoprolol most evidence), digoxin, hydralazine/ISDN, and diuretics (use caution)
53
# HF HF + breastfeeding considerations?
* BB can be used (metoprolol most evidence) * furosemide, spironolactone, captopril, enalapril, fosfinopril, quinalapril, and ramipril are also relatively safe * ACEi preferred over ARB and ARNI due to limited available data * avoid ivabradine due to no safety data
54
# HF NHP for HF? ## Footnote NHP = natural health product(s)
Omega-3 fatty acids. mixed outcomes, minimal evidence. Excessive bleeding at higher doses (> 3 g/d) - caution w/ antiplatelets and anticoagulants.
55
# HF Monitoring efficacy endpoints?
Sxs of HF (weight, fatigue, dyspnea, peripheral edema) should improve and stabilize within 2-3 days (diuretics improve fluid retention) to months (ACEi, BB effects).
56
# HF Monitoring safety endpoints?
* BP (> 90/60), HR, SCr, K (3.5-5), and Mg WNL, ongoing. Monitor more frequently in high risk individuals. * Prevent or minimize AEs of medications, ongoing.
57
# Misc Warfarin MOA
Acts as an indirect anticoagulant. Decreases ability of liver to produce coagulation factors II, VII, IX, X. Decreases ability of liver to produce endogenous anticoagulants such as protein C + S.
58
# Misc Common indications for warfarin
* stroke prevention in AF * treatment of VTE * long-term secondary prevention of VTE * VTE prevention in pts with mechanical heart valves
59
# Misc warfain dosing
Maintenance dose varies - anywhere from < 1 mg to > 20 mg daily Reasonable starting dose is 5 mg po daily, if frail or unerweight or of Asian descent - 1-2 mg po daily. Initiation with LMWH x 5 days and until INR is 2 x 2 days. Factors that affect the maintenence dose: age, weight, race, diet, genetic variation in VKOR + CYP2C9, drug interactions, EtOH, other disease states, level of daily activity
60
# Misc Monitoring warfarin
Routine lab monitoiring required for all warfarin patients. Target INR usually 2-3 (mechanical heart valve 2.5-3.5). Timeframe for INR change is 3-7 days, monitor no earlier than 2-3 days after initial dose or dose adjustment. Once stable, frequency can be reduced to once monthly.
61
# Misc Warfarin interactions
* Antiplatelet agents: risk of bleeding almost doubled. * NSAIDs: may use celecoxib or traditional NSAID + PPI to mitigate GI bleeding risk. * Abx: risk of increased INR * Acute infection: more frequent monitoring may be necessary * EtOH: may alter INR (both increased bleed risk or decreased anticoagulant effect possible) * supplements: SJW decreases anticoagulant effects, ginkgo increases bleed risk.
62
# Misc Warfarin reversal
Vitamin K * PO 2.5-10 mg - measure INR after 12-48h and administer subsequent dose PRN. Following PO admin, reversal expected in 6-10 hours, peak effect within 24-48h. * IV weight based dosing + Octaplex or Beriplex (four factor prothrombin complex) - dosing based on INR value or fixed. Measure INR at baseline and 30 mins post dose. Significant INR decline w/in 30 mins, maintained for up to 24+ hours.
63
# Misc Approach to out of range INR on warfarin
Questions to consider: * any missed doses in the past week? * started or stopped any meds/supplements recently? * changes in diet recently? Vitamin K rich foods. * changes in alcohol intake recently? transiently increase INR * current fever, diarrhea, flu, recent cold? higher INR than normal Consider single dose change if slighlty out of range INR (+/- 0.5) + transient cause identified - then repeat INR in 1-2 weeks. Change maintenence dose if 2 or more out of rance INR trending in the same direction.
64
# Misc Perioperative warfarin management
Bridging recommended if: mechanica mitral valve, older generation aortic valve, CHADS2 = 5 or 6, recent (last 3m) TIA/stroke/VTE/PE, prior VTE during inturruption of warfarin therapy. Bridging optional if: CHADS2 = 3 or 4, newer generation mechanical aortic valve, VTE in last 3-12m. IF bridging required - stop warfarin 5 days pre-op and obtain INR, use therapeutic LMWH for 3 days pre-op and administer in the morning. IF no bridging required - stop warfarin 5 days pre-op and obtain INR value.
65
# Syncope Patho of syncope
sudden temporary loss of conciousness. Reduction in venous blood flow to the heart (non-cardiac) --> decreased CO and BP --> impaired compensatory reflec response --> cerebral hypoperfusion --> syncope. Types: reflex, orthostatic hypotension, cardiac
66
# syncope Risk factors for syncope?
Fam hx, age > 70, previous CV events, emotional distress, medical conditions (CV disease, psychiatric conditions), medications (antihypertensives, diuretics, antianginals).
67
# syncope Clinical presentation of syncope
Prodromal: dizziness, lightheadedness, fatigue/weakness, visual disturbances, nausea, sweating/flushing syncope: loss of postural tone and concoiusness. Rapid and self-limiting. Complete recovery of consciousness. post-syncope attack: threat of reoccurance impairs QOL.
68
# syncope investigations for syncope
ECG to screen for cardiac syncope carotid sinus massage to screen for carotid sinus hypersensitivity (esp. in 50+) orthostatic hypotension screen complete Canadian Syncope Risk Score to risk stratify pts.
69
# syncope reflex sycope definition and tx
body overreacts to a trigger and cannot compensate for loss of oxygen to the brain (me w/ needles). Tx: * Non-pharm: education and reassurance, avoid triggers, recognize prodromal sxs, isometric counter-pressure maneuvers, fluid and salt intake increase (caution in renal/cardiac issues) * pharm: alpha-1-adrenergic agonist (midodrine), BB, mineralocorticoid (fludrocortisone), SSRIs (paroxetine)
70
# syncope orthostatic hypotension syncope definition and tx
hypotension when changing positions. May be caused by volume depletion, neurological disorders, or drugs. Tx: * non-pharm: education, reassurance, avoid offending agents, recognize prodromal sxs, isometric counter pressure maneuvers, sleep with head elevated (10 degrees), measure BP in all positions, increase fluid and salt intake (caution in kidney/heart issues). * alpha-1-adrenergic agonists (midodrine), mineralocorticoid (fludrocortisone), pyridostigmine, desmopressin, erythropoietin.
71
# syncope cardiac syncope definition and tx
various heart problems. * sinus node dyfx - pacemaker * AV block - pacemaker * paroxysmal supraventricular and ventricualr tachycardias - catheter ablation and/or antiarrhythmic agents, resolution of cause * structural heart disease - implantable cardioverter defibrilator, treat underlying disease
72
# syncope monitoring of efficacy endpoints for syncope
* reduce no. of episodes, ongoing. * eliminate orthostatic hypotension, ongoing. * prevent falls, ongoing.
73
# syncope monitoring of safety endpoints for syncope
* prevent/minimize supine hypertension, ongoing. * prevent/minimize other AEs, ongoing.
74
# Stroke/TIA Different types of strokes + differences between them?
**TIA:** disruption in blood flow to the brain resulting in damage. Neurological deficit lasting < 24 h (usually < 30 mins) and may be reversible. **Stroke**: Disruption in blood flow to the brain resulting in damage. Neurological deficit lasting > 24 h and may be irreversible. **Ischemic stroke**: occlusion of blood vessel supplying the brain. Penumbra is the area of reversible ischemia that can be saves in the first few hours after a stroke if treated properly. **Hemorrhagic stroke**: bleeding in the brain.
75
# Stroke/TIA Two origins of ischemic strokes?
* atherosclerotic origin - plaque * Cardioembolic - clot of cardiac origin
76
# Stroke/TIA Clinical presentation?
**FAST** - face drooping, arms raised, speech slurred, time to call 911. Sudden onset of weakness, numbness, tingling unilaterally, severe headache, agitation/delerium, slurred speach or trouble speaking, blurred vision, dizziness, spatial issues.
77
# Stroke/TIA Medication causes of strokes/TIAs?
Triptans and cocaine: vasospasm, HTN excess EtOH: presentation may resemble stroke; falls increase chance of hemorrhagic stroke. Anticoagulants: hemorrhagic stroke. HRT and OC: ischemic stroke. ## Footnote HRT = hormone replacement therapy, OC = oral contraception.
78
# Stroke/TIA Treatment algorithm for suspected stroke
Note time/LSN - perform CT/MRI, ECG, CBC, INR, glucose, lytes, SCr to determine if ischemic or hemorrhagic! * if ischemic: < 4.5 h since LSN? if no admit to stroke unit, if yes and pt meets t-PA criteria start t-PA. If yes and not eligible for t-PA but eligible for EVT do that. * if hemorrhagic - refer to neurosurgery or stroke unit. Control HTN and vasospasm. *note EVT can be performed in pts who have had alteplase (t-PA) tx* ## Footnote LSN = last seen normal, EVT = endovascular thrombectomy (EVT)
79
# Stroke/TIA Absolute CIs to alteplase?
* hemorrhagic stroke * condition that increases risk of hemorrhage after alteplase admin * hemorrhage on brain imaging.
80
# Stroke/TIA Relative CIs for alteplase
* **historical**: hx of ICH, stroke or serious head/spinal trauma w/in last 3m, major surgery in last 2w, arterial puncture at non-compressible site in last 7d. * **CT/MRI findings**: signs of extensive infarction * **Clinical**: sxs suggestive of subarachnoid hemorrhage, currently prescribed or taking DOAC, severe uncontrolled HTN (SBP > 185, DBP > 110) * **Labs**: BG < 2.7 or > 22.2, elevated PTT, INR > 1.7, platelet count < 100,000/mm3.
81
# Stroke/TIA HTN management post stroke
* pre-alteplase tx: aim for < 185/< 110 - labetalol 10mg IV (over 1-2 min), hydralazine 10 mg IV (over 1 min), NTG patch. * during/after alteplase tx: if SBP > 185/ > 110 for 2+ readings - continue IV labetolol, hydralazine, NTG patch. Add enalapril IV if needed. *Avoid aggressive decrease in BP as low BP increases risk of hypoperfusion*
82
# Stroke/TIA Acute antiplatelet therapy for stroke management
pts not on antiplatelet therapy pre-stroke and not getting alteplase should get ASA 160 mg as initial LD once brain imaging exclused hemorrhage then low dose ASA long-term for secondary prevention. In acute high-risk TIA or minor ischemic stroke of non-cardioembolic origin who are low bleed risk - DAPT w/ ASA and clopidegrel may be considered for first 3-4w. Pts receiving alteplase must wait until after the 24h post-thrombolysis CT scan to excluse intracranial hemorrhage (hemorrhagic transformation).
83
# Stroke/TIA Stroke prevention
Primary: lifestyle mod, BP (!!!), HbA1C < 7% Secondary: lipid managment w/ statin therapy in ischemic stroke/TIA pt (LDL < 1.8), initiate ACEi + thiazide diuretic once pt is stable post-stroke, initiate antiplatelet/anticoagulant therapy 24h after tPA administration once T excludes hemorrhage.
84
# Stroke/TIA Antiplatelet options post stroke?
* ASA: 75-325 mg has equal efficacy (81 mg po daily used most commonly) * Clopidegrel: concomitant PPI decreases efficacy.
85
# Stroke/TIA Monitoring efficacy endpoints for secondary prevention?
* BP < 130/80 w/in 2-3 weeks + ongoing * glucose fasting 4-7, PPG 5-10 w/in 1-2 weeks + ongoing * HbA1C < 7% w/in 3-6m + ongoing * LDL < 1.8 w/in 6-8 weeks + ongoing * prevent recurrent stroke/TIA ongoing.
86
# Stroke/TIA monitoring safety endpoints for secondary prevention?
* prevent AEs of antiplatelet/anticoagulant therapy, ongoing. * INR (if on warfarin) b/w 2-3 (2.5-3.5 if mechanical heart valve), ongoing.
87
# Raynauds What is Raynauds?
an extreme vascular response that discolours the affected area - generally follows a pattern of white to blue to red. 2 types: primary (less severe, more common, idiopathic) and secondary (underlying disease, drug induced). Blood vessels narrow causing limited blood flow to digits lasting seconds to hours followed by a hyperemia phase where blood flow returns to digits (red).
88
# Raynauds Clinical presentation of raynauds
The affected area may change colour and patient may feel throbbing, tingling, and burning. Can start in one digit and then spread symmetrically in both hands. More severe cases may result in skin sores, digital ulceration, gangrene. Clinical presentation and medical history is sufficient for diagnosis. Sxs usually decrease in frequency and intensity during pregnancy.
89
# raynauds Risk factors for raynauds
* general risk factors: Female, fam hx, age < 30, living in cold climate (e.g. frostbite), repetitive damage to arteries and nerves (e.g. carpal tunnel). * drugs: ergot derivatives, antineoplastics (e.g. bleomycin, cisplatin), interferon alfa, beta, CNS stimulants, cyclosporine, BBs * Occupational/recreational hazards: exposure to some chemicals (vinyl chloride, nicotine), vibration tools, repetitive actions. * Medical conditions: scleroderma, lupus, RA, atherosclerosis, sjogren's syndrome, hypothyroidism, pulmonary HTN
90
# Raynauds Non pharm options for raynauds
* avoid triggers: d/c offending meds if possible, lifestyle mods (smoking cessation, reduce caffeine, and EtOH intake), avoid vibrating tools and repetitive motions at work, stress reduction. * managing temperature: reduce exposure to temp extremes, especially cold, warm affected areas slowly, wear protectie clothing, place hands/affected area under warm water. * Physical activity: rotating arms like a windmills.
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# Raynauds Pharm options for raynauds
DHP-CCBs (nifedipine): * AEs: orthostatic hypotension, headache, dizziness, flushing, tachycardia, edema. * 1st line therapy: take 30-60 mins prior to being exposed to the cold. Take regularly during winter, reduce frequency not severity.
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# Raynauds Efficacy of raynauds treatment monitoring endpoints?
* prevent/reduce frequency of discolouration (white to blue to red) and throbbing, tingling, burning sensation in the first few days to 1 week. * Prevent skin sores, digital ulceration, gangrene, ongoing.
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# Raynauds safety monitoring of raynauds treamtment
* minimize or prevent AEs, ongoing.
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# HTN Types of HTN?
* essential HTN: > 130/80 * isolated systolic HTN: elevated SBP, normal DBP * white coat HTN: occurs only in clinical settings * masked HTN: normal BP in clinical settings, elevated elsewhere * HTN emergency: significant elevation in BP + organ damage * HTN urgency: significant elevation in BP but NO organ damage
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# HTN Complications of HTN?
* Brain: stroke, hypertensive encephalopathy * blood: elevated glucose * eye: hypertensive retinopathy * heart: MI, hypertensive cariomyopathy * kidneys: hypertensive nephhropathy
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# HTN CV risk factors?
* Non-modifiable (GRAF): gender, race, age (> 55), fam hx of premature CVD (< 55 in M, < 65 in F) * modifiable: smoking, EtOH, poor diet, high Na intake, sedentary, mental health, stress, poor DM control, chronic pain, non-adherence, obesity, sleep apnea.
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# HTN Drug and condition related causes of HTN
* drug: corticosteroids, NSAIDs, anabolic steroids, excessive EtOH intake, oral contraceptives, sex hormone, stimulants, atypical APs, decongestants (+ more) * condition: kidney/parathyroid disease, thyroid disease, pheochromocytoma, hyperaldosteronism, sleep apnea, obesity, cushings.
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# HTN How to measure BP properly at home
* rest in quiet place for 1-5 mins before measurments * sit on chair with back supported * feet flat on the ground, not crossed * no caffeine, tobacco, or exercise in the past 30 mins * ensure cuff size fits arm * arm bare, supported, and kept at heart level * take 3 readings, record, and average all * do not measure if stressed, cold, in pain, bowel/bladder full.
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# HTN High CVD risk criteria according to HTN canada
* established CVD * DM (type 1 + 2) * CKD (eGFR < 60 or albuminuria > 3 mg/mmol) * 10-year FRS 20%+ * age 75+
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# HTN SPRINT trial takeaway
* compared intensive BP control (< 120) reduced CV events compared to standard (< 140). * adults 50+ w/ SBP 130+ + increased CV risk (no DM or stroke) * intensive tx reduced rates of CV events (MI, stroke, HF) (25%) and all cause mortality (27%). Increased rates of hypotension, syncope, lyte abnormalities, and AKI.
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# HTN Diagnosing HTN
Mean out of office BP 130/80+ = HTN.
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# HTN Target for BP
Target is < 130 SPB
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# HTN When to treat vs when to watchful wait/lifestyle mod
if SBP 130-139 + not high CVD risk - lifestyle mods for 3-6 months. If SBP < 140/90 or < 130 + high CVD risk - promote health lifestyle mods and follow up q6-12m. if SBP 140/90+ OR 130-139 and high CVD risk - healthy lifestyle mods + meds: - step 1: low dose SPC w/ 2 of the following - ACEi/ARB, thiazide diuretic, LA-DHP CCB. - step 2: increase dose and reassess - step 3: triple therapy - step 4: spironolactone - step 5: specialist.
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# HTN Non-pharm measures for HTN
* weight control (BMI 18.5-24.9 + wasit circumfrence < 102 cm (40in) M and < 88 cm (35in) W. * smoking cessation * DASH diet * reduce EtOH consuption * Physical activity * reduce Na intake (< 2g/d) * increase dietary K if not at risk for hyperkalemia * relaxation therapies
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# HTN Thiazide diuretics considerations
long-acting (indapamide and chlorthalidone) preferred over short acting (HCTZ)
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# HTN LA-DHP CCBs considerations
amlodipine, consider risk of peripheral edema
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# HTN ACEi/ARB considerations
Caution in females of childbearing age and pts with hyperkalemia. Do NOT combine ACEi and ARBs.
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# HTN Special pops: HTN w/ DM AND one of - microalbuminuria, renal disease, CVD, or other CV risk factors
* 1st line - ACEi or ARB * 2nd line - DHP-CCB > thiazide
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# HTN special pops: HTN w/ DM w/o microalbuminuria, renal disease, CVD, or other CV risk factors
* 1st line - ACEi or ARB or thiazide * 2nd line - Combo of first line (if combo w/ ACEi then DHP-CCB preferred)
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# HTN Special pops: HTN + persons of African descent
NOT RECOMMENDED ACEi or ARB unless other compelling indicaitons (kidney protection, HF, or DM)
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# HTN Special pops: HTN + pregnancy
* 1st line - methyldopa, labetolol, LA-nifedipine. (other BBs may be considered - ace, met, pin, prop). * 2nd line - hydralazine, clonidne, thiazide * pre-eclampsia and eclampsia: IV mag, IV labetolol, IV hydralazine * ACEi/ARB teratogenic. * Severe HTN (BP 160/110+) is considered obstetrical emergency * target diastolic BP
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# HTN special pops: HTN + CAD (angina, MI)
* 1st line - BBs and ACEi (or ARB if ACEi not tolerated) * 2nd line - add LA-DHP CCB
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# HTN Special pops: HTN + HF
* 1st line - BB and ACEi (or ARB if ACEi not tolerated) * MRA may be added for non-HTN reasons * in HFrEF - ARNI > ACEi > ARB * 2nd line - hydralazine/ISDN combo if ACEi CI/not tolerated, thiazide or loop diuretics as additive therapy, DHP CCB, ARNI.
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# HTN special pops: HTN + past stroke/TIA
* 1st line - ACEi and thiazide
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# HTN special pops: HTN + non-DM CKD w/ proteinuria
* 1st line - ACEi (ARB if not tolerated) if proteinuria present. Diuretics as additive tx.
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# HTN monitoring efficacy endpoints for HTN
* SBP < 130 q1-3m until at target then q6-12m, ongoing
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# HTN monitoring safety endpoints for HTN
* minimal to no AEs from medications (dizziness, dry cough, peripheral edema), ongoing. * K levels within target 2-4 weeks after initiation and w/ any dose adjustment, ongoing. * SCr levels within target, ongoing depending on clinical scenario
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# HTN Troubleshooting poor response to therapy
possible reasons: * inaccurate BP measurement technique * suboptimal tx regimen * adherence * associated conditions * drug interactions