CARDIOLOGY Flashcards
differences between STEMI and NSTEMI
STEMI: ST elevation +elevated troponin. Complete occlusion of blood vessels resulting in necrosis of myocardium
NSTEMI: ST depression + elevated troponin, partial occlusion of blood vessels resulting in necrosis of myocardium
differences between stable and unstable angina
stable: exercise induced, no minimal ECG changes with no changes in troponin
unstable: often occurs while resting, sleeping or minimal physical activation. ST depression with no changes in troponin. Can lead to heart attack
symptoms of angina
chest heaviness, pressure, pain and discomfort.
chest symptoms may radiate to upper body, last <5 mins and received by rest or nitroglycerin
symptoms of ACS
same as angina but
lasting > 5 mins and not relieved by nitroglycerin
treatment for stable angina
chronic:
BB and/OR
NTG and/ OR
DPH ( long acting)
decreasing mortality:
anti platelet ( ASA or clopidogrel) statin
ACE-I or ARB
how many total dose of NG spray can u administer
total 3 doses
what condition does ACS compromise of
unstable angina
NSTEMI
STEMI
What is TIMI risk score ?
estimates mortality, recurrent MI or severe recurrent ischemia requiring urgent revascularization for patients with unstable angina and NSTEMI
high risk if TMI >/3
what medication to start post MI
A= ACE-I,
B- BETA BLOCKER
C- cholesterol - statin
D: DUAL ANTIPLALET
know treatment algorithms for UA/NSTEMI
SEE PIC
when would you choose fibrinolytic vs PCI
what is the absolute CI?
fibrinolytic: <1 hr presentation, when PCI is not an option, delay to invasive strategy
PCI: skilled PCI lab available, high risk STEMI, , late presentation >3 hrs, diagnosis in doubt
MOA of fibrinolytic?
CI?
altepase, tenecteplase
conversion of plasminogen to plasmin in the presence of of fibrin, resulting in fibrinolysis
any suspected hemorrhage or bleeding, known vascular lesion, or ischemic stroke within 3 months
know algorithm to STEMI
See pic
Which heparin should be used? how long should they be one this ?
UFH: STEMI patient receiving fibrinolytic.
LMWF ( enoxaparin has been shown to be superior to UFH in patients treated with tenecteplase
Heparins should be continued for a minimum of 48 hours ( or until PCI) and use can be extended in patients with high-risk features.
what is the MOA of UFH? AND AE?
potentiates antithrombin, inhibits factor Xa and IIa
AE: bleeding, HIT , osteoporosis
when should we initiate beta blocker ? what should the HR be?
BB in the first 24 hrs to all patient without contraindications,
Titrate to resting HR: 55-65 bpm
know duration of DAPT THERAPY
DAPT 1 year , if not at high risk of bleeding, continue DAPT for 3 years
if high risk after 1 year, SAPT ( ASA 81mg once daily or Clopidogrel 75 mg
when should be hold DAPT therapy for surgery
BMS: at least 1 month after PCI
DES: 3 months after PCI
switching between ticagrelor and prasugel?
prasugel to ticagrelor: no loading dose, ticagrelor 90 mg BID is recommended
Ticagrelor to prasugel: LD of 60 prasugel mg followed by 10 mg daily
switching from clopidogrel to ticagrelor or prasugel
clopidogrel to ticagrelor: LD ticagrelor of 180 mg followed by 90 mg BID
clopidogrel to prasugel: LD of 60mg followed by 10 mg regardless of timing of clopidogrel dose
when should u delay CABG surgery in patient taking ASA, clopidogrel , ticagrelor or prasugel?
ASA- continue
ticagrelor: 48-73 hrs (2-3 days) before CABG
clopidogrel: 48-73 hrs (2-3 days) before
prasugel: 5 dyas
patient with AF without high risk features who undergo elective PCI:
AGE < 65 AND CHAD2=0
ASA+ clopidogrel: at least 1 moth for BMS and 3 months for DES and up to 12 months
Age >/ 65 OR CHAD2>/1
OAC + clopidogrel ( 1 month for BMS and 3 months for DES)
AF + PCI FOR ACS or high risk elective PCI
AGE < 65 and CHAD2=0
ASA+ P2Y2 Inhibitor2 ( ticagrelor or prasugrel preferred over clopidogrel for ACS )- up to 12 months
AGE >/ 65 OR chads>/1
reduced OAC+ ASA+ Clopidogrel
ASA stop 1 day post PCI or anytime up to 6 months
followed by: clopidogrel + OAC up to 12 months
ACE-I and ARB AE
hypotension ( dizziness, headache), dry couch, hyperkalemia
ARB: similar to ACE but less dry cough and less angioedema
ACE- CI
pregnancy, bilateral renal artery stenosis, history of angioedema
list BB that are non-selective, selective , alpha blocking activity
non -selective: TPN ( Timolol, propanolol, nadolol)
B1 selective: Nebivolol, ABM (metoprolol, bisoprolol, atenolol) -
Non selective + ISA : pinolol
Selective + ISA: acetbutolol
with alpha blocking activity: labetalol
what the difference b/w different types of BB
B1 selective- less non cardiac AE due to B1 selectivity
alpha blocking activity: additional AE ( dizziness, edema, nasal congestion, postural hypotension)
DHP- CCB AE ?
hypotension, headache, peripheral edema, flushing, gingival hyperplasia ( amlodipine)
why is nifedipine not recommended
avoid short acting nifedipine because it increases risk of MI and death
NON-DHP CCB MOA and AE
Blocks voltage-gated calcium channels but are more cardio-selective than DHP-CCBS
constipation ( verapamil), anorexia, dizziness, bradycardia; heart bock, new or worsening heart failure
DI for NON-DHP CCB
strong CYP3A4 Inhibitors BBS antiarrhythmics ( digoxin, amiodarone) anti-hypertensives CYP3A4 substrates ( simvastatin) Verapamil can also increase digoxin levels
AE of clopidogrel? MOA?
MOA: P2Y12 inhibitor
diarrhea, rash, bleeding, purpura
AE of prasugel and CI?
increased bleeding risk, headache, nausea, dizziness
hypercholesterolemia, atrial fibrillation
CI: >75 years < 60kg, history of ischemic stroke
what are symptom of atrial fibrillation
palpitation, tachycardia, SOB, light headedness, syncope, decreased exercise capacity
describe different classification of atrial fibrillation ( paroxysmal, persistent, permanent/chronic )
paroxysmal: episodes lasting less than 30 seconds, terminating within 7 days ( spontaneous)
Persistent: lasting longer than 7 days up to 1 year
sinus rhythm restored by cardioversion or medications
permanent: continuous episode longer than 1 year, decision made not be pursue sinus rhythms restoration
what factors is included in CHADS-65 SCORE?
what is the score use for
CHF ( 1 POINT ) HTN ( 1 POINT AGE >/ 65 DIABETES STROKE (2 POINTS)
estimates risk of stroke in patient with afib
when would anti platelet be considered in AFIB?
< 65 YEARS, CHADS-65 <0 with CAD or PAD`
when would DOAC be preferred over warfarin?
NVAF: DOAC recommended
AF+ mechanical prosthetic valve or moderate mitral stenosis: warfarin
BB preferred in the presence of : LV dysfunction, hypertension, CAD
LV dysfunction: bisoprolol or carvedilol
hypertension: atenolol or metoprolol
CAD: atenolol, propanolol or metoprolol
which DOAC can be dose down to 15 ml/min
apixaban
DOAC that has high risk of dyspepsia
dabigatran
DOAC that is dose once daily
rivaroxaban and edoxaban
when will u dose apixaban 2.5mg BID
A: age > 80
B: body weight <60 mg
C: serum creatinine> 133mmol/ L
meet 2/3 criteria
MOA of warfarin
inhibitors VKORC1
affect factors 2,7,9,10 and protein C and S
when is rhythm control preferred
recently diagnosed AF ( within a year) highly symptomatic significant QOL impairment multiple recurrences difficult to achieve rate control arrthymia-induced cardiomyopathy
treatment for paroxysmal AF
low recurrence burden: observation + pill in pocket
which agent for rhythm control
Heart failure:
LVEF < 40%: amiodarone
LVEF > 40% amiodarone or sotalol
CAD : Amiodarone, dronedrone, sotalol
No HF or CAD: amiodarone, dronedrone, flecainide, propafenone, sotalol
WHICH BB is preferred in AF and LVEF < 40%
bisoprolol, carvedilol, metoprolol
can we used ND-CCB in LVEF < 40%
NO, you can used LVEF >40% ( diltiazem or verapamil)
CI of NDHP-CCB
pre-excitation, CHF, or LV dysnfuction
which AAD needs to be combine with AV-nodal blocking agent, why?
flecainide, propafenone, both can decrease the refractory period of the AV node, thereby increasing the ventricular rate
what is the pill in pocket strategy
flecainide or propafenone can be taken intermittently or as booster dose as outpatient
AE of digoxin
anorexia, N/V, weakness, dizziness, visual changes
explain virchow’s triad
hemodynamic changes: alteration in blood flow, blood stasis or turbulence
Hyper coagulable state: change in clotting functions that can be inherited of acquired
vascular injury: damage to the blood vessels’ endothelium, activates the coagulation cascade
treatment of HIT
start alternative agent: Lepirudin, fondaparinux, argatroban transition to warfarin once patient stabilized and platelets >100 000 /mm3
difference between LMWH and UFH
potentiates anti thrombin III inactivating thrombin ( as well as Xa) and preventing
conversion from fibrinogen to fibrin
more predictable anticoagulation dose response than UFH, decreased incidence of HIT, decrease need for routine monitoring and decrease major bleeding compared to heparin
antidote for UFH and LMWH
protamine sulphate
when is UFH preferred over LMWH
UFH in severe renal impairment, those at high risk of bleeding who may require rapid reversal and patient who have very recently received thrombolytic therapy
what is the role of fondaparinux
selective factor Xa inhibitor
better efficacy over heparins
does not require routine coagulation monitoring
** can be used in patient with current of history of HIT
treatment for VTE with dabigatran
cannot be used as initial therapy- use full dose of LMWH or hepairin for 5-10 days before switching to dabigatran 150mg PO BID
switching heparin, LMWF or warfarin to DOAC
No need to bridge with heparin or LMWF
for warfarin, start DOAC when INR <2 ( dabigatran and apixaban) or when INR <2.5 ( edoxaban) or INR < 2.5-3 ( rivaroxaban)
what are statin indicated conditions
LDL > 5.0 mol/ L
diabetes: age >40 years old, age >30 and DM x>/ 15year duration (Type 1 DM)
microvascular disease
CKD
Atherosclerotic cardiovascular disease ( ASCVD)
when should we initiate statin for primary prevention
(1) all high-risk patients (≥ 20% 10-year risk); or (2) intermediate-risk patients (10%-19.9%) when LDL-C is ≥ 3.5 mmol/L (or ApoB ≥ 1.05 g/L or non-HDL-C ≥ 4.2 mmol/L). among intermediate-risk individuals men 50 years of age or older or women 60 years of age or older with 1 additional risk factor including low HDL-C, impaired fasting glucose, increased waist circumference, cigarette smoking, hypertension)
then statin indicated conditions
should u start statin on patient on dialysis
no, but if they are already on statin at that time, it can be continue
when should we consider PCSK9 ihbitiors
alirocumba and evolocumab
considered in very high-risk individuals (patients with familial hypercholesterolemia or in secondary cardiovascular prevention) whose lipid targets have not been reached with maximally tolerated lipid-lowering medication
has greater LDL lowering than statin
MOA of statin: AE?
CI?
inhibit HMG CoA reductase
Myalgia, GI, headache, dizziness, increased CK and transaminases
CI: pregnancy, active liver disease
can statin be used in pregnancy or breast feeding
no
MOA of ezetimibe , AE
inhibits intestinal cholesterol absorption
AE: back pain, arthralgia, diarrhea, abdominal pain, fatigue, dizziness, headache.
MOA of fibres and AE?
increased activity of PPARa which results in an increased of lipid metabolism
AE: Upper GI disturbances (nausea, abdominal pain, flatulence), myalgias.
MOA of cholesteramine, AE?
conselling points?
binds to bile acids in the GI tract
constipation (>10%), bloating, abdominal fullness, flatulence
counsel: Administer other drugs 1 h before or 4–6 h after resin to limit possible reduced absorption in the GI tract.
when is fenofibrate useful
high TG >2.3 mmol and low HDL-C
what is 3 types heart failure
impaired inability to fill with ( diastole) or eject ( systole) blood
1: HF with preserve LVEF ( diastolic dysfunction): filling problems due to HTN ( LVEF >/50%)
2: HF with midrange EF ( LVEF 41-49%)
3: HF with reduced LVEF ( systolic dysfunction): pumping problems ( <40% )
to compensate for decrease CO, body respond with 4 mechanisms
1: stimulation of RAAS: retains water and constricts blood vessels ( increase after load and preload)
2: increased SV ( stroke volume) to increase CO ( increase preload)
3: enlarging ventricular walls to increase Force of contract ( hypertrophy)
4: Increased HR to increased CO ( preload and after load)
symptoms of hF
hypotension, dyspnea, systemic congestion, peripheral edema
non-pharm treatment for HF
salt restriction ( <2-3 g of Na+/day) fluid restriction: 2L/ day from all sources monitor weight treat risk factors: HTN, diabetes ( risk of HF reduced by 50% by managing HTN along :)
know NYHA function classification of HF
I: No symptoms with ordinary activity
II: Symptoms occur with ordinary activity ( SOB)
III: Symptoms occur with less than ordinary activity
IV: Symptoms occur at rest or with minimal activity
What is treatment for midrange and persevere EF
symptomatic relieve: diuretic for congestion and managing risk factors
treatment for HF-rEF
ACE-I OR ARB OR ARNI
BB ( metoprolol, carvedilol and bisoprolol)
MRNA
SGLT2I ( dapa and empa)
what is the role of ivabradine?
sinus rhythm with a resting heart rate ≥77 bpm
what is the role of nitrates/ hydralazine
reduces mortality and morbidity in black patients with NYHA class III–IV HF and is recommended in addition to standard therapy (ACE inhibitor, beta-blocker with or without MRA) in this settin
which ARBs showed decreased in mortality with HF
candesartan and valsartan
switching from ACE-I to ARNI
washout period of 36h required when switching from ACE to ARNI but no washout required when switching from ARB
what is the role of digoxin in HF? what is the usual dose range
** does not reduce mortality
considered in Ventricular rate control in patient with AF not controlled on BB or who cannot tolerate BB
0.0625–0.25 mg daily
target trough levels for digoxin and when should we measure them
Measure trough serum concentrations at least 8 hours after administration and adjust the dose to maintain the serum concentration between 0.6 and 1.2 nmol/L
which drug do not show reduce mortality in HF
diuretics ( furosemide)
digoxin
what is systolic and diastolic BP
systolic: heart muscles contract causing elevated BP since blood is pumped out of the heart
diastolic: heart muscle relaxes and decrease BP as blood fills the heart
know values for:
isolated systolic HTN
hypertensive emergency
hypertensive urgency
isolated: >140/ <90 mmhg
emergency: >180/120 mmHg with organ damage
hypertensive urgency: >180/120 mmhg and no organ damage
what is blood pressure?
BP= cardiac output (CO) x systemic vascular resistance ( SVR)
explain the RAAS system
kidney releases renin in response to hypotension, sympathetic stimulation and decreased blood flow to the kidneys
angiotensin II: increased cardiac contractility and CO
increased aldosterone synthesis–> increased Na/H20
vasoconstriction –> increased SVR ( systemic vascular resistance)
resistant hypertension
bp above target while on 3 or more BP at optimal doses
what is defined as hypertension HIGH RISK patient
50 years old AND SBP 130-190 AND one or more of the following:
clinical or sub clinical cardiovascular disease OR CKD OR estimated 10-year global cardiovascular risk >/ 15% OR 75 years old
threshold for intitation of antihypertensive therapy
hypertension high risk patient AND Treatment target
> 130/ N/A
target <120/ N/A
threshold for intitation of DM patient AND Treatment target
threshold: >/ 130/ 80
goal <130/ 80
threshold for intitation of moderate-to-high risk patient and LOW risk AND Treatment target
moderate-high risk
threshold: >/140/ 90
goal < 140/90
low risk
threshold >160/100
goal: <140/ 90
1st line HTN treatment in patient without other compelling indications
thiazide /thiazide like diuretics ACEI ARB LA-CCB BB
HTN+ DM+ (microalbuminaria, renal disease, CVD Or other CV risk: 1st and 2nd line
1st: ACEI-ARB
2ND: addition of of DHP-CCB over thiazide/ thiazide like diuretic
HTN in African american patient
ACEI/ARB not preferred unless other compelling indications ( kidney production or HF)
HTN and pregnancy?
1st: methyldopa, labetalol, long acting nifedipine, and other BB
2nd: hydralazine, clonidine or other thiazide diuretics PO
Difference between TIA and stroke
TIA: disruption in blood flow to the brain resulting in damage
neurological deficit lasting <24 hr ( usually <30 mins) and may be reversible
Stroke: same as TIA but neurological deficit lasting >24 hrs and may be irreversible
treatment of stroke?
alteplase
what is the criteria for administering alteplase
administer alterplase within 4.5 hrs of symptoms onset
d\
what is Alteplase CI
any source of active hemorrhage or any condition that could increase the risk of major hemorrhage after altepase
what is the dose of apletplase
0.9 mg/kg to max of 90mg infused over 60 mins
target door to alteplase
less than 60 mins
When would u administer ASA
Administered ASA 160mg at least 24 hrs AFTER tPA once CT excludes intracranial hemorrhage
would u aggressive lower BP in stroke>
what should BP be after alteplase
no, it will cause hypo-perfusion
BP should be lowered and maintained below 185/110 before altephase and kept below 180/105 mmHg for the next 24 hrs after
What is the single most important modifiable risk factor for stroke
BP
1st line treatment for raynaud phenomenons
DHP- CCB
60 mins before exposure to the cold
Alpha 1 adrenergic prazosin
Regular usage to avoid syncope/orthostasis
Alternative:
PDE5
Treatment for supra ventricular arrthymia
procainamide
what is orthostatic hypotension
drop in systolic BP >20mmHg or diastolic BP >10 mmHg when sitting to an upright position.
Treatment for Orthostatic hypotension
midodrine, fludrocortisone
warfarin INR range
2-3
mechanical valvue 2.5-3.5
when should u check INR after dose adjustment
no earlier than 2-3 days ( INR change normally 3-7 days)
factors that can change INR
1) antibiotics, azole antifungals, synthroid dose changes can increase INR
vitamin K rich foods ( green leafy vegetables, soy, avocado)
alcohol
current fever, diarrhea, flu, recent cold
Liver Disease can increase INR
when should u stop warfarin for preoperative which does require bridging
stop 5 das pre- op and obtain INR value on POD-1, use therapeutic LMWH for about 3 days pre-op, last pre-op LMWF dose should be 24 hrs Pre op
MOA of thiazide and AE?
MOA: Na+ CI- co- transporter inhibition in the kidney tubules
AE: diuresis, hypokalemia ( decrease Cl, mg,
increase Ca, hyperuricemia
MOA of loop diuretics and AE
bumetanide, furosemide
AE: hypokalemia, increased urinary frequency and dehydration
Which drug belongs to vasodilators and AE
Hydralazine, isosorbide, nitroglyerin,
Dilation of blood vessels and smooth muscle relaxation
AE: headache, fushing, hypotension and syncope,
what are significant drug interactions with vasodilators
PDE-5 inhibitors ( sildenafil drugs)
what is the MOA of doxazosin, prazosin, and terazosin? AE?
peripheralalpha 1 adrenergic receptors inhibitors
AE: postural hypotension, headache & palpatations,
MOA of methyldopa?
stimulation of central alpha adrenergic receptors
MOA of ivabradine?
inhibition If which results in decrease heart rate
HR has to be what to administer ivabradine
HR > 70 BPM
MOA of digoxin and AE
inhibits Na-K ATpase
GI (N/V/D)
fatigue and dizziness
Bradycardia; AV blocks
which BB also belong to CLASS III antiarrythmic
sotalol
disadvantage of UFH which limits its used
narrow therapeutic range, need for lab monitoring and increased risk of HIT
if patient previous had HIT, which alternative drug can be used
fondaparinux due to lack of immune mediated effect on platelets, always still use with caution
antidote for UFH and LMWH
Protamine sulphate
what the loading dose of clopidogrel should be in a patient with ST-elevation myocardial infarction (STEMI).
300-600mg
Which of the following drugs are NOT recommended in ST-elevation myocardial infarction (STEMI)?
Calcium channel blockers increase morbidity and mortality in patients with STEMI and are not recommended. They may be used cautiously to relieve ischemia or to achieve rate control in patients with atrial fibrillation if beta-blockers are contraindicated.
what is the MAX dose tenecteplase
The recommended total dose should not exceed 50 mg and is based upon patient weight.
Which of the following laboratory tests is MOST indicative of myocardial injury?
troponin
what are important contraindication of BB
severe bradycardia ( <50bpm)
2nd and 3rd degree AV block
severe hypotension
**ASTHMA is not a CI
(LMWHs) have the Health Canada approved indication for the treatment of acute ST-segment elevation myocardial infarction (STEMI)?
enoxaparin
Which of the following lab values should be monitored every 6-12 months for patients taking direct oral anticoagulants (DOACs)?
Serum creatinine (SCr). It is prudent for patients who are receiving a DOAC to have an assessment of kidney function, hemoglobin and platelet count every 6-12 months and with any acute medical illness, since worsening of renal function may warrant a change in the dose of a DOAC,
Which of the following oral anticoagulants has a once daily dosing regimen for stroke prevention in non-valvular atrial fibrillation?
Rivaroxaban
pre-operative management of DOAC and post operative
in low-moderate bleeding risk: give last dose 2 days before procedure
in high risk: give last dose 3 days before surgery ** except for dabigatran, give last dose 5 days before surgery
resume on day after surgery ** 24 hrs post operative
what does HAS-BLED stand for
H: hypertension A: abnormal liver/ renal function S: stroke history B: bleeding L: labile INR E: elderly ( >./ 65) D: drug/alcohol usage
what important DI should we be aware of with DOAC
Drugs that inhibit P-gp can INcrease systemic exposure to DOACs and increase risk of bleeding. Concomitant use of the strong P-gp inhibitors (e.g., ketoconazole) and apixaban, dabigatran and rivaroxaban is contraindicated.
is regular lab work required for LMWH
no
which type of diet will ELEVATE or DECREASE INR with warfarin
elevate: cranberry juice
decrease: food high in vitamin K including green leafy vegetables
what would be considered a good TTR ( time to therapeutic range)
> 60%
can acetaminophen affet iNR
yes, increase in dose >1-2 g/day
The ability of the left ventricle to return blood to the systemic circulation is expressed via:
EF ( ejection fraction)
which drug should we avoid in HF
Avoid diltiazem and verapamil in patients with HFrEF because of their negative inotropic effects, and felodipine and nifedipine because of the lack of data
list the most potent to least potent diuretics
furosemide? metalozone > HCTZ> spironolactone
what is the role of nitrates and hydralazine ( H-ISDN in HF)
unable to tolerate an ACEI, ARB, or ARNI because of hyperkalemia, renal dysfunction
addition to standard guideline-directed medical therapy at appropriate doses for black patients with HFrEF and advanced symptoms
Which of the following medications have been shown to reduce hospitalizations in patients with heart failure with preserved ejection fraction (HFpEF)?
ARB
Which of the following laboratory finding(s) indicates fluid overload in a patient with heart failure?
BNP
Most common cause of HF
CAD ( ischemic)
what is the benefit of spironolactone ins patient with post MI
Spironolactone has been shown to reduce mortality in post-MI patients with severe LV dysfunction.
How long should dual antiplatelet therapy (DAPT) be used after a medically managed ST-elevation myocardial infarction in the absence of contraindications to ASA or a high risk of bleeding?
14 DAYS
** Whereas, DAPT is indicated for 12 months when percutaneous intervention is used to manage a STEMI or NSTEMI.
Don’t think this slide is right..
How long should dual antiplatelet therapy (DAPT) be used after a medically managed NSTEMI n the absence of contraindications to ASA or a high risk of bleeding?
1 MONTH
What is the most common cause of cardioembolic stroke?
aFIB
switching from DOAC to warfarin
stop apixaban, edoxaban and rivaroxaban and use bridging agent ( enoxaparin) with warfarin until iNR is achieved
** there has been guidlines which mentioned overlapping dabigatran with warfarin until INR achieved
When should we initiated icosapent ethyl
TG> 1.5 to 5.6 mmol/L
Which agent is most potent in decreasing TG
Fibrates
